Relation Results

Identifier	Residue	Organism	Cell Line
SIGNOR-251935		Homo sapiens	Epithelial Ovarian Cancer Cell
pmid	sentence
15531507	Nodal induces apoptosis and inhibits proliferation in human epithelial ovarian cancer cells via activin receptor-like kinase 7.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-255648
pmid	sentence
23290138	This result strongly supports the assertion that Wnt7a and FN stimulate PCP signaling to drive the symmetric expansion of satellite stem cells during regenerative myogenesis.

Publications:

1

Pathways:

Acute Myeloid Leukemia, FLT3-ITD in AML, WNT Signaling, WNT/FLT3

Identifier	Residue	Organism	Cell Line
SIGNOR-259089		Homo sapiens	Calu-1 Cell
pmid	sentence
27626682	Conversely, in Calu-1 cells, which express higher endogenous levels of the receptor, siRNA-mediated LRP1B knockdown significantly enhanced cellular proliferation. Taken together, these findings demonstrate that, consistent with the postulated tumor suppressor function, overexpression of full-length Lrp1b leads to impaired cellular proliferation, while LRP1B knockdown has the opposite effect.

Identifier	Residue	Organism	Cell Line
SIGNOR-259091		Homo sapiens	SW-480 Cell, SW-620 Cell
pmid	sentence
28408316	Forced expression of LRP1B in SW480 and SW620 cells inhibited the growth, migration and anchorage-independent growth of cancer cells.

Publications:

2

Organism:

Homo Sapiens

Identifier	Residue	Organism	Cell Line
SIGNOR-261246		Homo sapiens	Hep-G2 Cell
pmid	sentence
23325603	MAT2B and GIT1 regulate cell growth and increase ERK activity.GIT1 and MAT2B (V1 and V2) require one another to regulate growth and activate ERK

Identifier	Residue	Organism	Cell Line
SIGNOR-261242		Homo sapiens	U2-OS Cell
pmid	sentence
30942439	MAT2B Promotes Proliferation and Inhibits Apoptosis in Osteosarcoma by Targeting Epidermal Growth Factor Receptor and Proliferating Cell Nuclear Antigen

Publications:

2

Organism:

Homo Sapiens

Identifier	Residue	Organism	Cell Line
SIGNOR-256260		Homo sapiens	NCI-H292 Cell, NCI-H1299 Cell, A-549 Cell, NCI-H460 Cell, SK-MES-1 Cell
pmid	sentence
23725574	Our data suggested that increased expression of BAD enhance apoptosis and has negative influence on cell proliferation and tumor growth in NSCLC. Bad is a new potential target for tumor interventions.

Publications:

1

Organism:

Homo Sapiens

Pathways:

Acute Myeloid Leukemia, COVID-19 Causal Network, FLT3-ITD in AML, FLT3-ITD signaling, Malignant Melanoma, VEGF Signaling

Identifier	Residue	Organism	Cell Line
SIGNOR-256265		Homo sapiens	KKU-100 Cell
pmid	sentence
28599455	The results demonstrated that NQO1 siRNA-mediated knockdown effectively impaired colony formation capacity, induced cell cycle arrest at the G1 phase and suppressed migration of KKU-100 cells.

Identifier	Residue	Organism	Cell Line
SIGNOR-256264		Homo sapiens	Melanoma Cell Line
pmid	sentence
20226854	More importantly, our results also indicate that NF-kappaB p50 correlates with the expression of NQO1 and mediates its role in the proliferation of melanoma cells.

Publications:

2

Organism:

Homo Sapiens

Pathways:

Hepatocellular Tumor

Identifier	Residue	Organism	Cell Line
SIGNOR-256205		Homo sapiens	Urinary Bladder Cancer Cell
pmid	sentence
30518913	This study show that UBIAD1 interacts with H-Ras, retains H-Ras in the Golgi apparatus, prevents H-Ras trafficking from the Golgi apparatus to the plasma membrane, blocks the aberrant activation of Ras/MAPK signaling, and inhibits the proliferation of bladder cancer cells.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-254374		Homo sapiens
pmid	sentence
24743741	Activation of PDGFRα stimulates proliferation of PDGFRα(+) cells through PI3K-Akt and MEK2-MAPK signaling pathways, and aberrant accumulation of PDGFRα(+) cells was conspicuous in muscles of patients with both genetic and non-genetic muscle diseases.

Identifier	Residue	Organism
SIGNOR-255120		Mus musculus
pmid	sentence
20219869	Furthermore, stimulation of myoblasts with CCL2, CCL3, or CCL4 was sufficient to induce phosphorylation and activation of ERK1/2. This outcome may be functionally important because ERK1/2 activation is a component of the pathway through which many mitogenic growth factors can stimulate cell proliferation.

Identifier	Residue	Organism
SIGNOR-256216		Homo sapiens
pmid	sentence
20219869	ERK1/2 activation is a component of the pathway through which many mitogenic growth factors can stimulate cell proliferation

Identifier	Residue	Organism	Cell Line
SIGNOR-255580		Homo sapiens	Monocyte
pmid	sentence
11602185	The GM-CSF promoted cell survival and proliferation correlated with MEK-1 dependent ERK1/2, Elk-1 and CREB phosphorylation and Egr-1, c-Fos expression as well as with increased STAT-5, AP-1, c-Myb and NF-kappaB DNA-binding.

Identifier	Residue	Organism
SIGNOR-254354		Homo sapiens
pmid	sentence
19819937	In addition to the JAK2–STAT5 pathway, the Ras GTPase–extracellular signal-regulated kinase (Ras–ERK) pathway has also been implicated in signaling of IL-5 and is important for IL-5-dependent cell survival, proliferation and differentiation of eosinophils.

Publications:

5

Organism:

Homo Sapiens, Mus Musculus

Tissue:

Skeletal Muscle

Pathways:

Acute Myeloid Leukemia, BCR-ABL in AML, FLT3 in AML, KIT in AML, AML_TRIPLETS, AMPK Signaling, B-cell activation, COVID-19 Causal Network, Colorectal Carcinoma, EGFR Signaling, ErbB receptors in cancer, FLT3-ITD in AML, FLT3-ITD signaling, Glioblastoma Multiforme, Hepatocellular Tumor, IL6 Signaling, Insulin Signaling, Integrin Signaling, Luminal Breast Cancer, Leptin Signaling, Malignant Melanoma, Triple mutant AML, NPM1_new, Non-small-cell lung cancer (NSCLC), Pancreatic ductal adenocarcinoma (PDA), PI3K/AKT Signaling, Rhabdomyosarcoma, RTKs in cancer, SARS-CoV MAPK PERTURBATION, Thyroid cancer, VEGF Signaling, WNT/FLT3

Identifier	Residue	Organism
SIGNOR-255412		Homo sapiens
pmid	sentence
18177723	Cyclin D1 is necessary for proliferation of different cell types, including myogenic cells.

Identifier	Residue	Organism	Cell Line
SIGNOR-260014		Homo sapiens	Hepatocyte
pmid	sentence
11731443	Cyclin D1 regulates mitogen-dependent progression through G1 phase in cultured cells, and its overexpression in malignant cells is thought to contribute to autonomous proliferation in vivo.

Publications:

2

Organism:

Homo Sapiens

Pathways:

Acute Myeloid Leukemia, DNMT3A in AML, AML_TRIPLETS, Triple mutant AML

Identifier	Residue	Organism
SIGNOR-255695		Homo sapiens
pmid	sentence
23645839	For example, prostaglandin E2 (PGE2), 1 of the major metabolites downstream of both COX-1 and COX-2, has been shown to activate β-catenin–dependent signaling in hematopoietic stem cells (HSCs) and promote HSC expansion

Identifier	Residue	Organism
SIGNOR-255654		Homo sapiens
pmid	sentence
18697834	we showed that β-catenin, a key component of the canonical Wnt-signalling cascade, is present in quiescent satellite cells in the inactive form, but subsequently becomes activated following satellite-cell activation. This observation suggests that the proliferation initiated by the Wnt-signalling cascade does not have to rely on transcription of β-catenin, but rather on activation of this protein, which is already present within the quiescent satellite cells.

Publications:

2

Organism:

Homo Sapiens

Pathways:

Acute Myeloid Leukemia, AML1-ETO in AML, FLT3 in AML, Onco-fusion proteins in AML, Colorectal Carcinoma, FLT3-ITD in AML, FLT3-ITD signaling, Hepatocellular Tumor, Pancreatic ductal adenocarcinoma (PDA), PPARgamma in cancer, Retinoic acid Signaling, Rhabdomyosarcoma, Thyroid cancer, Wnt in cancer, WNT Signaling, WNT/FLT3

Identifier	Residue	Organism	Cell Line
SIGNOR-256295		Homo sapiens	Melanoma Cell
pmid	sentence
17148680	Here we investigated the effects of HO-1 overexpression in murine and human melanoma cells. The most important findings of our study are that 1) overexpression of HO-1 augments the proliferation [.]

Publications:

1

Organism:

Homo Sapiens

Pathways:

Hepatocellular Tumor

Identifier	Residue	Organism	Cell Line
SIGNOR-259107		Homo sapiens	MCF-10A Cell, Mammary Epithelial Cell Line, MDA-MB-231 Cell
pmid	sentence
26079538	In addition, enhanced AF1q expression promotes breast cancer cell proliferation, migration, mammosphere formation, and chemo-resistance.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-255643
pmid	sentence
17495111	In summary, the absence of Myf5 clearly reduced the initial expansion of satellite cell-derived transient amplifying cells and resulted in a shift of the ratio of satellite cell subpopulations but did not affect the specification and generation of specific subpopulations of satellite cell-derived cells such as reserve cells, amplifying cells, and differentiating mature myogenic cells.

Publications:

1

Tissue:

Skeletal Muscle

Identifier	Residue	Organism
SIGNOR-255414		Homo sapiens
pmid	sentence
21408055	We have demonstrated that following muscle damage, phosphorylated STAT3 (p-STAT3) in SCs increases early (within one hour), inducing downstream target genes (i.e. GP130 and SOCS3), which further regulate the increase in STAT3 production and response (as induced via IL-6), leading to increased cMyc expression, which drives cell proliferation

Identifier	Residue	Organism
SIGNOR-259110		Mus musculus
pmid	sentence
7882978	These observations indicate that continued late-stage expression of L-myc affected differentiation processes directly, rather than indirectly through deregulated growth control, whereas constitutive c-myc expression inhibited proliferative arrest, but did not appear to disturb differentiation.

Identifier	Residue	Organism
SIGNOR-56572		Homo sapiens
pmid	sentence
9552384	C-myc has emerged as one of the central regulators of mammalian cell proliferation.

Publications:

3

Organism:

Homo Sapiens, Mus Musculus

Tissue:

Skeletal Muscle, Lens Fiber

Pathways:

Acute Myeloid Leukemia, AML1-ETO in AML, BCR-ABL in AML, DNMT3A in AML, FLT3 in AML, KIT in AML, miRNA in AML, MLL fusion protein in AML, NPM1 in AML, AML_TRIPLETS, Colorectal Carcinoma, EGFR Signaling, FLT3-ITD in AML, FLT3-ITD signaling, Hepatocellular Tumor, mTOR in cancer, Triple mutant AML, NPM1_new, Prostate Cancer, Rhabdomyosarcoma, Thyroid cancer, Wnt in cancer, WNT Signaling, WNT/FLT3

Identifier	Residue	Organism
SIGNOR-245043		Homo sapiens
pmid	sentence
11359934	The nuclear factor-kappaB (NF-kappaB) family of transcription factors has been shown to regulate proliferation in several cell types.

Identifier	Residue	Organism
SIGNOR-255692		Homo sapiens
pmid	sentence
22021368	In normal hematopoiesis, AML1 suppresses NF-κB signaling and thus may contribute to inhibition of excessive proliferation of hematopoietic cells.

Publications:

2

Organism:

Homo Sapiens

Pathways:

Acute Myeloid Leukemia, miRNA in AML, B-cell activation, COVID-19 Causal Network, EBV infection, FLT3-ITD signaling, Glucocorticoid receptor Signaling, NF-KB Canonical, Pancreatic ductal adenocarcinoma (PDA), TNF-alpha Signaling

Identifier	Residue	Organism
SIGNOR-256015		Mus musculus
pmid	sentence
17494859	MN1 is a unique oncogene in hematopoiesis that both promotes proliferation/self-renewal and blocks differentiation, and may become useful as a predictive marker in AML treatment.

Publications:

1

Organism:

Mus Musculus

Identifier	Residue	Organism
SIGNOR-260048		Homo sapiens
pmid	sentence
11494141	Flow cytometry suggested that over-expression of BPOZ inhibited progression of the cell cycle at the G1/S transition. Anti-sense oligonucleotides for BPOZ or EGR2 effectively inhibited their expression, and cell growth was accelerated.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism	Cell Line
SIGNOR-259149		Homo sapiens	U2-OS Cell
pmid	sentence
30403180	Osteosarcoma is the most common malignant bone tumor with high incidence in adolescence and poor prognosis. RBM10, a member of RBPs, was reported to be a tumor suppressor in many kinds of cancers. The results showed that U2OS cell growth was significantly inhibited when RBM10 is overexpressed as compared with negative control cells.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-262532		Homo sapiens
pmid	sentence
21524151	In its hypophosphorylated state, pRb binds transcription factors of the E2F family which are required for cell cycle progression. As the level of CyclinD/Cdk4/6 complexes increases, pRb becomes phosphorylated and progression through G1 occurs. At a critical level of phosphorylation, E2F is released from pRb. This activates the transcription of CyclinE which complexes with Cdk2 to fully release pRb repression by further phosphorylation, establishing a positive feedback loop. E2F further promotes the transcription of S-phase genes. Thus, CyclinD/Cdk4/6 and CyclinE/Cdk2 together regulate S-phase entry via phosphorylating pRb, which controls pRb binding to E2F

Publications:

1

Organism:

Homo Sapiens

Pathways:

FLT3-ITD signaling, Integrin Signaling

Identifier	Residue	Organism	Cell Line
SIGNOR-256266		Homo sapiens	Hep-G2 Cell
pmid	sentence
15730925	PKC-alpha asODN (antisense oligonucleotides) could inhibit the growth and proliferation of HepG2 and induce its apoptosis by blocking the cell signal transduction related to PKC-alpha in vitro, and may be potentially used in the prevention and management of recurrent and metastatic HCC.

Publications:

1

Organism:

Homo Sapiens

Pathways:

B-cell activation, VEGF Signaling

Identifier	Residue	Organism
SIGNOR-259139		Homo sapiens
pmid	sentence
26997225	Overexpression of MGLL inhibits proliferation and delays cell cycle progression in QGY-7703 cells. Forced overexpression of MGLL in human HCC cells resulted in marked inhibition in cell proliferation with a significant delay in cell cycle progression [.]

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-255944		Homo sapiens
pmid	sentence
20508131	The mammalian target of rapamycin complex 1 (mTORC1) integrates mitogen and nutrient signals to control cell proliferation and cell size.

Identifier	Residue	Organism
SIGNOR-255108		Homo sapiens
pmid	sentence
15829723	Phosphorylation of mTOR by Akt leads to mTOR activation (40, 52) and the subsequent activation of p70S6K (47). This latter event has great potential importance for the promotion of muscle growth by the IGF-I/Akt/mTOR pathway, because p70S6k is a potent stimulator of protein synthesis that can be activated by increases in muscle contraction

Publications:

2

Organism:

Homo Sapiens

Tissue:

HEK-293 Cell, Skeletal Muscle

Pathways:

Acute Myeloid Leukemia, BCR-ABL in AML, FLT3 in AML, IDH-TET in AML, KIT in AML, miRNA in AML, FLT3-ITD in AML, FLT3-ITD signaling, Glioblastoma Multiforme, Leptin Signaling, Pancreatic ductal adenocarcinoma (PDA)

Identifier	Residue	Organism
SIGNOR-260046		Homo sapiens
pmid	sentence
11494141	Flow cytometry suggested that over-expression of BPOZ inhibited progression of the cell cycle at the G1/S transition. Anti-sense oligonucleotides for BPOZ or EGR2 effectively inhibited their expression, and cell growth was accelerated.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism	Cell Line
SIGNOR-265550		Homo sapiens	Keratinocyte
pmid	sentence
31836722	Epidermal expression of axonemal dynein heavy chain 10 (DNAH10) was increased 20-fold in samples having had regenerating dermis vs control. Our results associate DNAH10 expression with cell proliferation and inflammation as well as with the epidermal memory resulting from the previous regenerative signals of dermis.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-229764		Homo sapiens
pmid	sentence
17081971	The interaction of beta-catenin with the N terminus of tcf/lef transiently converts it into an activator, translating the Wnt signal into the transient transcription of Tcf target genes. The Wnt pathway has distinct transcriptional outputs, which are determined by the identity of the responding cell, and range from cell proliferation and survival to the terminal differentiation of postmitotic cells.

Publications:

1

Organism:

Homo Sapiens

Pathways:

Colorectal Carcinoma, Hepatocellular Tumor, Wnt in cancer, WNT Signaling, WNT/FLT3

Identifier	Residue	Organism
SIGNOR-255360		Homo sapiens
pmid	sentence
20219869	Prostaglandins are able to affect muscle cell proliferation (142), differentiation (96) and fusion (141), and can also modulate muscle fiber growth and the synthesis and degradation of proteins in muscle

Identifier	Residue	Organism
SIGNOR-255362		Homo sapiens
pmid	sentence
3308494	The results suggest a role for prostanoids in the regulation of both human myoblast proliferation and differentiation

Publications:

2

Organism:

Homo Sapiens

Tissue:

Skeletal Muscle

Identifier	Residue	Organism
SIGNOR-199217		Homo sapiens
pmid	sentence
23075495	Yap and taz are two main downstream effectors of the hippo pathway, and they function as transcription co-activators to promote cell proliferation and inhibit apoptosis.

Publications:

1

Organism:

Homo Sapiens

Pathways:

Hippo in cancer, Hippo Signaling, Integrin Signaling

Identifier	Residue	Organism
SIGNOR-254302		Homo sapiens
pmid	sentence
10072077	Here, we demonstrate that, while lymphoid development is normal, Stat5a/b mutant peripheral T cells are profoundly deficient in proliferation and fail to undergo cell cycle progression or to express genes controlling cell cycle progression

Identifier	Residue	Organism	Cell Line
SIGNOR-255682		Homo sapiens	Culture Condition:CD34+ Cell
pmid	sentence
15353555	Here we report that a persistent activation of STAT5A in human CD34+ cells results in enhanced self-renewal. STAT5A drives the expression of a number of proto-oncogenes and cytokines in human CD34+ cells, as well as a number of erythroid-specific genes, favoring erythroid over myeloid differentiation and providing a long-term proliferative advantage for erythroid progenitors.

Identifier	Residue	Organism	Cell Line
SIGNOR-256233		Homo sapiens	Mast Cell
pmid	sentence
20535135	Specifically, SCF-induced activation of JAK2 in human mast cells has been shown to activate STAT5 and STAT6. STAT5 contributes to mast cell homeostasis, by mediating proliferation, survival, and mediator release.

Publications:

3

Organism:

Homo Sapiens

Pathways:

Acute Myeloid Leukemia, AML1-ETO in AML, BCR-ABL in AML, FLT3 in AML, Onco-fusion proteins in AML, KIT in AML, miRNA in AML, AML_TRIPLETS, B-cell activation, FLT3-ITD in AML, FLT3-ITD signaling, Glucocorticoid receptor Signaling, Leptin Signaling, Triple mutant AML

Identifier	Residue	Organism	Cell Line
SIGNOR-261687		Homo sapiens	SGC-7901 Cell
pmid	sentence
22343731	The results of the MTT assay and growth curves revealed that the cells transfected with pEGFP-p27kip1 had a significant growth inhibition when compared with cells transfected with pEGFP-NC (Fig. 5B and D). These data indicated that overexpression of p27kip1 could arrest cell-cycle progression and decrease proliferation of SGC-7901 cells.

Publications:

1

Organism:

Homo Sapiens

Pathways:

Acute Myeloid Leukemia, IDH-TET in AML, Integrin Signaling

Identifier	Residue	Organism
SIGNOR-265886		Homo sapiens
pmid	sentence
30154312	GREB1 is an early estrogen-responsive gene, and its expression is correlated with estrogen levels in breast cancer patients. Additionally, GREB1 responds to androgen in prostate cancer cells, and can stimulate the proliferation of breast, ovarian, and prostate cancer cells.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-199211		Homo sapiens
pmid	sentence
23075495	Yap and taz are two main downstream effectors of the hippo pathway, and they function as transcription co-activators to promote cell proliferation and inhibit apoptosis.

Publications:

1

Organism:

Homo Sapiens

Pathways:

Hippo in cancer, Hippo Signaling, Integrin Signaling

Identifier	Residue	Organism	Cell Line
SIGNOR-255577		Homo sapiens	Monocyte
pmid	sentence
19436055	Low pM concentrations of GM-CSF mediate βc Ser585 phosphorylation, leading to 14-3-3 binding, PI-3 kinase activation, and hemopoietic cell survival, whereas at concentrations of 10 pM or more, GM-CSF mediates βc Tyr577 phosphorylation, Shc recruitment, and PI-3 kinase activation, thereby promoting both survival and proliferation.

Publications:

1

Organism:

Homo Sapiens

Tissue:

Skeletal Muscle

Pathways:

Acute Myeloid Leukemia, ASXL1 in AML, BCR-ABL in AML, FLT3 in AML, Onco-fusion proteins in AML, KIT in AML, B-cell activation, COVID-19 Causal Network, EBV infection, ErbB receptors in cancer, FLT3-ITD in AML, FLT3-ITD signaling, Hepatocellular Tumor, Integrin Signaling, Leptin Signaling, mTOR in cancer, Non-small-cell lung cancer (NSCLC), Pancreatic ductal adenocarcinoma (PDA), PI3K/AKT Signaling, RTKs in cancer, VEGF Signaling, WNT/FLT3

Identifier	Residue	Organism	Cell Line
SIGNOR-259109		Homo sapiens	Neural Stem Cell Line
pmid	sentence
27546534	Our findings demonstrate that stable expression of the L-MYC gene in NSC008 cells promotes their survival and proliferation while preserving their migration and differentiation properties in vitro and in vivo.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-266700		Homo sapiens
pmid	sentence
23977024	Depletion of TBCK significantly inhibits cell proliferation, reduces cell size, and disrupts the organization of actin, but not microtubule.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-263651		Homo sapiens
pmid	sentence
21433395	The signal transducer and activator of transcription (STAT) family of transcription factors transduce signals from a variety of extracellular stimuli, and are important mediators of inflammation, cell survival, differentiation, and proliferation. STATs are activated in response to growth factors, cytokines, and G-CSF binding to cell surface receptor tyrosine kinases. Although structurally similar, the seven STAT family members possess diverse biological roles. For example, STAT1 activation is pro-inflammatory and anti-proliferative, while STAT3 activation is anti-inflammatory and pro-apoptotic.

Publications:

1

Organism:

Homo Sapiens

Pathways:

EGFR Signaling, EBV infection, P38 Signaling

Identifier	Residue	Organism	Cell Line
SIGNOR-252938		Homo sapiens	HEK-293 Cell
pmid	sentence
14976264	Sirt1 increased foxo3's ability to induce cell cycle arrest and resistance to oxidative stress

Publications:

1

Organism:

Homo Sapiens

Pathways:

Acute Myeloid Leukemia, BCR-ABL in AML, FLT3 in AML, IDH-TET in AML, FLT3-ITD in AML, FLT3-ITD signaling, NPM1_new, PI3K/AKT Signaling

Identifier	Residue	Organism
SIGNOR-256003		Homo sapiens
pmid	sentence
25428262	We have shown that SF3B1 knockdown in four myeloid cell lines resulted in inhibition of cell growth and disruption of the cell cycle.Taken together, these data show that SF3B1 knockdown results in inhibition of cell growth, induction of cell cycle arrest and impairment of erythroid differentiation in myeloid cell lines.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-254372		Homo sapiens
pmid	sentence
24743741	Activation of PDGFRα stimulates proliferation of PDGFRα(+) cells through PI3K-Akt and MEK2-MAPK signaling pathways, and aberrant accumulation of PDGFRα(+) cells was conspicuous in muscles of patients with both genetic and non-genetic muscle diseases.

Publications:

1

Organism:

Homo Sapiens

Pathways:

FLT3-ITD signaling, Glioblastoma Multiforme

Identifier	Residue	Organism	Cell Line
SIGNOR-255669		Homo sapiens	Fibroblast
pmid	sentence
7667317	P53 controls both the G2/M and the G1 cell cycle checkpoints and mediates reversible growth arrest in human fibroblasts

Publications:

1

Organism:

Homo Sapiens

Pathways:

Acute Myeloid Leukemia, AML1-ETO in AML, DNMT3A in AML, Onco-fusion proteins in AML, IDH-TET in AML, KIT in AML, miRNA in AML, NPM1 in AML, AML_TRIPLETS, Colorectal Carcinoma, EBV infection, FLT3-ITD in AML, FLT3-ITD signaling, Luminal Breast Cancer, Malignant Melanoma, Triple mutant AML, NPM1_new, Non-small-cell lung cancer (NSCLC), P38 Signaling, Prostate Cancer, Pancreatic ductal adenocarcinoma (PDA)

Identifier	Residue	Organism	Cell Line
SIGNOR-256262		Homo sapiens	Hep-G2 Cell
pmid	sentence
26194347	Nrf2 was up-regulated in HCC, and expression of Nrf2 was correlated with tumor differentiation, metastasis, and tumor size. Further studies demonstrated that inhibition of Nrf2 expression inhibited proliferation by inducing apoptosis and repressed invasion, and up-regulation of Nrf2 expression resulted in opposite phenotypes.

Publications:

1

Organism:

Homo Sapiens

Pathways:

Hepatocellular Tumor

Identifier	Residue	Organism
SIGNOR-261213		Mus musculus
pmid	sentence
24663380	Using a shRNA KD approach, we show thatÂ Ano6-KD C2C12 myoblasts exhibit reduced proliferation capacity. Our data demonstrate that Ano6 is required to maintain the proliferative status of myoblasts.

Publications:

1

Organism:

Mus Musculus

Identifier	Residue	Organism
SIGNOR-256482		Mus musculus
pmid	sentence
23582327	Activation of IL-4/IL-13 signaling promotes proliferation of FAPs to support myogenesis while inhibiting their differentiation into adipocytes

Publications:

1

Organism:

Mus Musculus

Identifier	Residue	Organism
SIGNOR-255895		Mus musculus
pmid	sentence
16415155	We also found that menin is important for the proliferation of MLL oncoprotein-transformed myeloid cells, pointing to a paradoxically oncogenic role for the tumor suppressor menin in proliferation of transformed myeloid cells.

Publications:

1

Organism:

Mus Musculus

Pathways:

Acute Myeloid Leukemia, Onco-fusion proteins in AML, MLL fusion protein in AML

Identifier	Residue	Organism	Cell Line
SIGNOR-260077		Mus musculus	32D Cell
pmid	sentence
15169904	Pescadillo (PES1) and the upstream binding factor (UBF1) play a role in ribosome biogenesis, which regulates cell size, an important component of cell proliferation. We have investigated the effects of PES1 and UBF1 on the growth and differentiation of cell lines derived from 32D cells, an interleukin-3 (IL-3)-dependent murine myeloid cell line. Parental 32D cells and 32D IGF-IR cells (expressing increased levels of the type 1 insulin-like growth factor I [IGF-I] receptor [IGF-IR]) do not express insulin receptor substrate 1 (IRS-1) or IRS-2. 32D IGF-IR cells differentiate when the cells are shifted from IL-3 to IGF-I. Ectopic expression of IRS-1 inhibits differentiation and transforms 32D IGF-IR cells into a tumor-forming cell line. We found that PES1 and UBF1 increased cell size and/or altered the cell cycle distribution of 32D-derived cells but failed to make them IL-3 independent. PES1 and UBF1 also failed to inhibit the differentiation program initiated by the activation of the IGF-IR, which is blocked by IRS-1. 32D IGF-IR cells expressing PES1 or UBF1 differentiate into granulocytes like their parental cells. In contrast, PES1 and UBF1 can transform mouse embryo fibroblasts that have high levels of endogenous IRS-1 and are not prone to differentiation. Our results provide a model for one of the theories of myeloid leukemia, in which both a stimulus of proliferation and a block of differentiation are required for leukemia development.

Publications:

1

Organism:

Mus Musculus

Pathways:

Acute Myeloid Leukemia, MLL fusion protein in AML

Identifier	Residue	Organism
SIGNOR-252356		Homo sapiens
pmid	sentence
9878062	AP‐1 proteins, including c‐Fos and c‐Jun, are prominent nuclear targets of growth factor induced signaling, making AP‐1 a candidate nuclear effector of growth factor induced proliferation.

Publications:

1

Organism:

Homo Sapiens

Pathways:

Acute Myeloid Leukemia, AML1-ETO in AML, FLT3 in AML, Onco-fusion proteins in AML, miRNA in AML, B-cell activation, COVID-19 Causal Network, EBV infection, FLT3-ITD signaling, Hepatocellular Tumor, Luminal Breast Cancer, Leptin Signaling, Pancreatic ductal adenocarcinoma (PDA), SARS-CoV MAPK PERTURBATION, TGF-beta Signaling, TGFb in cancer

Identifier	Residue	Organism
SIGNOR-255872		Homo sapiens
pmid	sentence
21389315	Consequently, cell cycle and apoptosis analyses suggest that MLL-AF4 conveys a selective proliferation coupled to a survival advantage, which correlates with changes in the expression of genes involved in apoptosis, sensing DNA damage and DNA repair.

Publications:

1

Organism:

Homo Sapiens

Pathways:

Acute Myeloid Leukemia, miRNA in AML, MLL fusion protein in AML

Identifier	Residue	Organism
SIGNOR-259135		Homo sapiens
pmid	sentence
30365124	SND1 upregulation is a common phenomenon in different human malignant tissues. We found that SND1 overexpression significantly promoted cell proliferation and tumor growth in vitro and in vivo.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-255552		Homo sapiens
pmid	sentence
14617280	Cell proliferation is highly dependent on the synthesis of polyamines, which are derived from arginine metabolism

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism	Cell Line
SIGNOR-255632		Homo sapiens	Satellite Cell
pmid	sentence
18177723	Altogether, these data demonstrate that IL-6 loss results in deficient STAT3 signaling in activated satellite cells, leading to their reduced proliferation and myogenic progression, and highlight the major role played by the IL-6/STAT3 axis in controlling these processes during compensatory hypertrophy.

Identifier	Residue	Organism	Cell Line
SIGNOR-245048		Homo sapiens	Satellite Cell
pmid	sentence
25194572	STAT3 signaling controls satellite cell expansion and skeletal muscle repair

Identifier	Residue	Organism	Cell Line
SIGNOR-256256		Homo sapiens	Mesenchymal Stem Cell
pmid	sentence
30029643	In summary, our results indicate IL-15 can stimulate the proliferation of FAPs through Jak-STAT pathway.

Publications:

3

Organism:

Homo Sapiens

Tissue:

Skeletal Muscle

Pathways:

Acute Myeloid Leukemia, KIT in AML, EGFR Signaling, EBV infection, FLT3-ITD signaling, IL6 Signaling, Leptin Signaling, Pancreatic ductal adenocarcinoma (PDA), Rhabdomyosarcoma

Identifier	Residue	Organism
SIGNOR-251540		Homo sapiens
pmid	sentence
15861399	AR homodimers recruit a panoply of factors including coactivators and mediator proteins whose enzymatic activities promote chromatin remodeling and transcriptional regulation of target genes leading to cell differentiation, survival, and proliferation

Publications:

1

Organism:

Homo Sapiens

Pathways:

Prostate Cancer

Identifier	Residue	Organism
SIGNOR-256230		Homo sapiens
pmid	sentence
30029643	In summary, our results indicate IL-15 can stimulate the proliferation of FAPs through Jak-STAT pathway.

Publications:

1

Organism:

Homo Sapiens

Pathways:

EGFR Signaling, Pancreatic ductal adenocarcinoma (PDA)

Identifier	Residue	Organism	Cell Line
SIGNOR-260133		Homo sapiens	Acute Myeloid Leukemia Cell
pmid	sentence
24183681	These data demonstrate an HSC cell intrinsic role for Sox4 on proliferation induced by loss of C/EBPα.

Publications:

1

Organism:

Homo Sapiens

Pathways:

Acute Myeloid Leukemia, AML1-ETO in AML, FLT3 in AML, AML_TRIPLETS, Triple mutant AML

Identifier	Residue	Organism	Cell Line
SIGNOR-255859		Homo sapiens	Leukemia Cell
pmid	sentence
19109563	These results show that MEIS1 expression is important for MLL-rearranged leukemias and suggest that MEIS1 promotes cell-cycle entry.Flow cytometric analysis of PI-stained nuclei showed that Meis1 knockdown led to a cell-cycle arrest in the G0/G1 phase.

Publications:

1

Organism:

Homo Sapiens

Pathways:

Acute Myeloid Leukemia, DNMT3A in AML, MLL fusion protein in AML, AML_TRIPLETS, Triple mutant AML

Identifier	Residue	Organism
SIGNOR-255551		Homo sapiens
pmid	sentence
14617280	Cell proliferation is highly dependent on the synthesis of polyamines, which are derived from arginine metabolism

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism	Cell Line
SIGNOR-256011		Mus musculus	Bone Marrow Cell
pmid	sentence
26847029	Our results strongly suggest that BCOR plays an indispensable role in hematopoiesis by inhibiting myeloid cell proliferation and differentiation and offer a mechanistic explanation for how BCOR regulates gene expression such as Hox genes.

Publications:

1

Organism:

Mus Musculus

Pathways:

Acute Myeloid Leukemia, MLL fusion protein in AML

Identifier	Residue	Organism
SIGNOR-254353		Mus musculus
pmid	sentence
16982699	Protein kinase B (PKB/Akt) is an important modulator of insulin signaling, cell proliferation, and survival. Using small interfering RNA duplexes in nontransformed mammalian cells, we show that only Akt1 is essential for cell proliferation

Identifier	Residue	Organism
SIGNOR-257606		Homo sapiens
pmid	sentence
24743741	Activation of PDGFRα stimulates proliferation of PDGFRα(+) cells through PI3K-Akt and MEK2-MAPK signaling pathways, and aberrant accumulation of PDGFRα(+) cells was conspicuous in muscles of patients with both genetic and non-genetic muscle diseases.

Publications:

2

Organism:

Mus Musculus, Homo Sapiens

Pathways:

Acute Myeloid Leukemia, ASXL1 in AML, BCR-ABL in AML, FLT3 in AML, KIT in AML, miRNA in AML, AML_TRIPLETS, AMPK Signaling, B-cell activation, COVID-19 Causal Network, EGFR Signaling, EBV infection, ErbB receptors in cancer, FLT3-ITD in AML, FLT3-ITD signaling, Glioblastoma Multiforme, Hepatocellular Tumor, Insulin Signaling, Integrin Signaling, Luminal Breast Cancer, Leptin Signaling, mTOR in cancer, Malignant Melanoma, Triple mutant AML, NPM1_new, Non-small-cell lung cancer (NSCLC), Prostate Cancer, Pancreatic ductal adenocarcinoma (PDA), PI3K/AKT Signaling, Rhabdomyosarcoma, RTKs in cancer, Thyroid cancer, VEGF Signaling, WNT/FLT3

Identifier	Residue	Organism	Cell Line
SIGNOR-259406		Homo sapiens	Carcinoma Cell
pmid	sentence
7972006	Transfection of the p16INK4 cDNA expression vector into carcinoma cells inhibits their colony-forming efficiency and the p16INK4 expressing cells are selected against with continued passage in vitro. These results are consistent with the hypothesis that p16INK4 is a tumor-suppressor protein and that genetic and epigenetic abnormalities in genes controlling the G1 checkpoint can lead to both escape from senescence and cancer formation.

Publications:

1

Organism:

Homo Sapiens

Pathways:

Acute Myeloid Leukemia, AML1-ETO in AML, ASXL1 in AML, DNMT3A in AML, Onco-fusion proteins in AML, NPM1 in AML, Luminal Breast Cancer, Malignant Melanoma, Triple mutant AML, NPM1_new, Pancreatic ductal adenocarcinoma (PDA), Rhabdomyosarcoma, TGFb in cancer

Identifier	Residue	Organism	Cell Line
SIGNOR-260136		Homo sapiens	Acute Myeloid Leukemia Cell
pmid	sentence
19516275	Hexamethylene bis-acetamide inducible protein 1 (HEXIM1) inhibits the positive transcription elongation factor b (P-TEFb), which is a key RNA polymerase II (Pol II) transcriptional regulator. In transfected cells, mutated NPM1 associated with, and sequestered, HEXIM1 in cytoplasm, resulting in higher transcription of RNA pol II target genes, among which were some positive regulators of cell-cycle progression such as cyclin D1 and anti-apoptotic proteins such as Mcl-1

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism	Cell Line
SIGNOR-256296		Homo sapiens	A-549 Cell
pmid	sentence
29928434	Accordingly, downregulation of GSTA1 suppressed tumor growth. In conclusion, GSTA1 plays an important role in regulation of cell proliferation and cell apoptosis in A549 cell line.

Publications:

1

Organism:

Homo Sapiens

Pathways:

Hepatocellular Tumor

Identifier	Residue	Organism	Cell Line
SIGNOR-255705		Homo sapiens	HL-60 Cell
pmid	sentence
25601757	Cell proliferation was stimulated by the knockdown of either TET2 or WT1 gene in KG-1 cells, but not additively by the co-depletion of both genes. Collectively, these results suggest that TET2 and WT1 function in the same pathway to inhibit leukemia cell proliferation and colony formation.

Publications:

1

Organism:

Homo Sapiens

Pathways:

AML-IDH/TET, Acute Myeloid Leukemia, DNMT3A in AML, Onco-fusion proteins in AML, AML-IDH/TET, IDH-TET in AML, miRNA in AML, NPM1_new

Identifier	Residue	Organism
SIGNOR-255553		Homo sapiens
pmid	sentence
14617280	Cell proliferation is highly dependent on the synthesis of polyamines, which are derived from arginine metabolism

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism	Cell Line
SIGNOR-261685		Mus musculus	32D Cell
pmid	sentence
9710637	PLZF expression in 32DG/GM cells is associated with growth suppression and G1 arrest.

Publications:

1

Organism:

Mus Musculus

Pathways:

Acute Myeloid Leukemia, FLT3-ITD in AML

Identifier	Residue	Organism	Cell Line
SIGNOR-259088		Homo sapiens	NCI-H1703 Cell, A-549 Cell
pmid	sentence
22549160	The small GTPase Rac1 regulates many cellular processes, including cytoskeletal reorganization, cell migration, proliferation, and survival. We found that silencing of Rac1 expression decreases NSCLC migration and proliferation [.]

Publications:

1

Organism:

Homo Sapiens

Pathways:

Acute Myeloid Leukemia, FLT3-ITD in AML, WNT Signaling, WNT/FLT3

Identifier	Residue	Organism	Cell Line
SIGNOR-260078		Mus musculus	32D Cell
pmid	sentence
15169904	Pescadillo (PES1) and the upstream binding factor (UBF1) play a role in ribosome biogenesis, which regulates cell size, an important component of cell proliferation. We have investigated the effects of PES1 and UBF1 on the growth and differentiation of cell lines derived from 32D cells, an interleukin-3 (IL-3)-dependent murine myeloid cell line. Parental 32D cells and 32D IGF-IR cells (expressing increased levels of the type 1 insulin-like growth factor I [IGF-I] receptor [IGF-IR]) do not express insulin receptor substrate 1 (IRS-1) or IRS-2. 32D IGF-IR cells differentiate when the cells are shifted from IL-3 to IGF-I. Ectopic expression of IRS-1 inhibits differentiation and transforms 32D IGF-IR cells into a tumor-forming cell line. We found that PES1 and UBF1 increased cell size and/or altered the cell cycle distribution of 32D-derived cells but failed to make them IL-3 independent. PES1 and UBF1 also failed to inhibit the differentiation program initiated by the activation of the IGF-IR, which is blocked by IRS-1. 32D IGF-IR cells expressing PES1 or UBF1 differentiate into granulocytes like their parental cells. In contrast, PES1 and UBF1 can transform mouse embryo fibroblasts that have high levels of endogenous IRS-1 and are not prone to differentiation. Our results provide a model for one of the theories of myeloid leukemia, in which both a stimulus of proliferation and a block of differentiation are required for leukemia development.

Publications:

1

Organism:

Mus Musculus

Identifier	Residue	Organism	Cell Line
SIGNOR-256298		Homo sapiens	G-401 Cell
pmid	sentence
12226744	The hSNF5/INI1 gene encodes a member of the SWI/SNF chromatin remodelling complexes.Here, we show that the ectopic expression of wild-type hSNF5/INI1, but not that of truncated versions, leads to a cell cycle arrest by inhibiting the entry into S phase of MRT cells.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-256306		Mus musculus
pmid	sentence
26728554	Hhex is a potential therapeutic target that is specifically required for AML stem cells to repress tumor suppressor pathways and enable continued self-renewal.

Publications:

1

Organism:

Mus Musculus

Tissue:

Blood

Pathways:

Acute Myeloid Leukemia, FLT3 in AML

Identifier	Residue	Organism	Cell Line
SIGNOR-256201		Homo sapiens	MDA-MB-231 Cell, NCI-H1299 Cell
pmid	sentence
30455429	NR4A3 exhibits p53-independent anti-proliferative functions. Ectopic expression of NR4A3 inhibits the growth of MDA-MB-231 and H1299 cancer cell lines.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-261324
pmid	sentence
22685333	ATF2 contributes to global transcription and the DNA damage response, in addition to specific transcriptional activities that are related to cell development, proliferation and death.

Publications:

1

Pathways:

COVID-19 Causal Network, SARS-CoV MAPK PERTURBATION, TGF-beta Signaling

Identifier	Residue	Organism	Cell Line
SIGNOR-255704		Homo sapiens	HL-60 Cell
pmid	sentence
25601757	Cell proliferation was stimulated by the knockdown of either TET2 or WT1 gene in KG-1 cells, but not additively by the co-depletion of both genes. Collectively, these results suggest that TET2 and WT1 function in the same pathway to inhibit leukemia cell proliferation and colony formation.

Publications:

1

Organism:

Homo Sapiens

Pathways:

AML-IDH/TET, Acute Myeloid Leukemia, DNMT3A in AML, AML-IDH/TET, IDH-TET in AML, miRNA in AML, NPM1_new

Identifier	Residue	Organism
SIGNOR-256064		Homo sapiens
pmid	sentence
15829723	Phosphorylation of mTOR by Akt leads to mTOR activation (40, 52) and the subsequent activation of p70S6K (47). This latter event has great potential importance for the promotion of muscle growth by the IGF-I/Akt/mTOR pathway, because p70S6k is a potent stimulator of protein synthesis that can be activated by increases in muscle contraction

Identifier	Residue	Organism
SIGNOR-256063		Homo sapiens
pmid	sentence
20508131	The mammalian target of rapamycin complex 1 (mTORC1) integrates mitogen and nutrient signals to control cell proliferation and cell size.

Publications:

2

Organism:

Homo Sapiens

Tissue:

Skeletal Muscle, HEK-293 Cell

Pathways:

AMPK Signaling, EGFR Signaling, Glioblastoma Multiforme, Insulin Signaling, Luminal Breast Cancer, mTOR in cancer, Pancreatic ductal adenocarcinoma (PDA), PI3K/AKT Signaling, WNT/FLT3

Identifier	Residue	Organism
SIGNOR-268044		Homo sapiens
pmid	sentence
19219026	Here we report that the c-Myc (hereafter referred to as Myc) oncogenic transcription factor, which is known to regulate microRNAs and stimulate cell proliferation, transcriptionally represses miR-23a and miR-23b, resulting in greater expression of their target protein, mitochondrial glutaminase, in human P-493 B lymphoma cells and PC3 prostate cancer cells.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-266114		Homo sapiens
pmid	sentence
33361741	Kinesin Family Member C1 (KIFC1) Regulated by Centrosome Protein E (CENPE) Promotes Proliferation, Migration, and Epithelial-Mesenchymal Transition of Ovarian Cancer

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism	Cell Line
SIGNOR-259407		Mus musculus	Myeloid Leukemia Cell
pmid	sentence
14681685	The Ink4b gene (Cdkn2b) encodes p15Ink4b, a cyclin-dependent kinase inhibitor. It has been implicated in playing a role in the development of acute myeloid leukemia (AML) in man, since it is hypermethylated with high frequency. We provide evidence that the gene is a tumor suppressor for myeloid leukemia in mice.

Publications:

1

Organism:

Mus Musculus

Pathways:

Pancreatic ductal adenocarcinoma (PDA), TGF-beta Signaling, TGFb in cancer

Identifier	Residue	Organism	Cell Line
SIGNOR-261728		Homo sapiens	KG-1 Cell, HL-60 Cell
pmid	sentence
30283340	Overexpression of MYCT1 Inhibits Proliferation and Induces Apoptosis in Human Acute Myeloid Leukemia HL-60 and KG-1a Cells in vitro and in vivo

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-255376
pmid	sentence
12361602	Taken together, these results show that Notch-1 activity promotes myogenic cell proliferation and that attenuation of Notch-1 activity by its antagonist Numb causes cells to exit from the cell cycle, express MRFs, and undergo myogenic differentiation.

Publications:

1

Tissue:

Skeletal Muscle

Pathways:

Acute Myeloid Leukemia, FLT3-ITD in AML

Identifier	Residue	Organism
SIGNOR-266854		Homo sapiens
pmid	sentence
31746409	Overexpression of CACNA2D3 reduced proliferation and migration, but increased apoptosis and Ca2+ influx in Ishikawa and RL95-2 cells.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism	Cell Line
SIGNOR-255722		Homo sapiens	U-937 Cell
pmid	sentence
8394219	We expressed the PML-RARa protein in U937 myeloid precursor cells and showed that they lost the capacity to differentiate under the action of different stimuli (vitamin Ds and transforming growth factor pl), acquired enhanced sensitivity to retinoic acid, and exhibited a higher growth rate consequent to diminished apoptotic cell death.

Publications:

1

Organism:

Homo Sapiens

Pathways:

Acute Myeloid Leukemia, FLT3 in AML, Onco-fusion proteins in AML

Identifier	Residue	Organism
SIGNOR-255745		Homo sapiens
pmid	sentence
15824134	Inhibition of p38 / MAPKs (a) promotes exit from the cell cycle, (b) prevents differentiation, and (c) insulates the cell from most external stimuli allowing the satellite cell to maintain a quiescent state. Activation of satellite cells and p38 / MAPKs occurs concomitantly, providing further support that these MAPKs function as a molecular switch for satellite cell activation

Publications:

1

Organism:

Homo Sapiens

Tissue:

Skeletal Muscle

Pathways:

FLT3-ITD signaling, Glucocorticoid receptor Signaling, P38 Signaling, TNF-alpha Signaling, TGF-beta Signaling

Identifier	Residue	Organism
SIGNOR-264239		Homo sapiens
pmid	sentence
26206665	MDGA2 acts as a novel tumour suppressor in gastric cancer through inhibiting cell proliferation, suppressing G1–S cell cycle transition and inducing cell apoptosis.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism	Cell Line
SIGNOR-259099		Homo sapiens	SH-EP Cell
pmid	sentence
21385898	Our findings define properties of CAMTA1 in growth suppression and neuronal differentiation that support its assignment as a 1p36 tumor suppressor gene in neuroblastoma.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism	Cell Line
SIGNOR-255734		Homo sapiens	ML-1 Cell
pmid	sentence
15829981	SiRNA mediated silencing of cyclin A1 in highly cyclin A1 expressing ML1 leukemic cells significantly slowed S phase entry, decreased proliferation and inhibited colony formation.

Publications:

1

Organism:

Homo Sapiens

Pathways:

Acute Myeloid Leukemia, ASXL1 in AML, FLT3 in AML, Onco-fusion proteins in AML

Identifier	Residue	Organism
SIGNOR-256371		Homo sapiens
pmid	sentence
22260161	We have previously shown that PER2 is a downstream CCAAT-enhancer-binding protein (C/EBP)-target gene, and its disruption might be involved in the initiation and progression of acute myelogenous leukemia (AML)

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-251562		Homo sapiens
pmid	sentence
24470334	TBX2 blocks myogenesis and promotes proliferation in rhabdomyosarcoma cells

Publications:

1

Organism:

Homo Sapiens

Pathways:

Rhabdomyosarcoma

Identifier	Residue	Organism
SIGNOR-255575		Homo sapiens
pmid	sentence
24890514	Socs1 associates with CSF-1R pTyr-697 and pTyr721 binding sites to inhibit proliferation by an unknown mechanism

Publications:

1

Organism:

Homo Sapiens

Pathways:

IL6 Signaling

Identifier	Residue	Organism
SIGNOR-233467		Homo sapiens
pmid	sentence
9878062	Functional data suggest that c-Jun is not merely a target for activation by many of the extracellular stimuli, but that it plays a role in mediating the cellular response. In the case of growth control, three lines of evidence suggest that the transcription factor AP-1, which is composed of FosJun and JunJun dimers, mediates cell proliferation in response to external growth signals in the form of peptide growth factors.

Publications:

1

Organism:

Homo Sapiens

Pathways:

Acute Myeloid Leukemia, AML1-ETO in AML, EGFR Signaling, Glioblastoma Multiforme, Glucocorticoid receptor Signaling, Insulin Signaling, Luminal Breast Cancer, TNF-alpha Signaling, TGF-beta Signaling, WNT Signaling, WNT/FLT3

Identifier	Residue	Organism
SIGNOR-241614		Mus musculus
pmid	sentence
26470845	Consistently, our results show that ASXL1 mutations are associated with lower expression levels of p15INK4B and a proliferative advantage of hematopoietic progenitors in primary bone marrow cells, and that depletion of ASXL1 in multiple cell lines results in resistance to growth inhibitory signals.

Publications:

1

Organism:

Mus Musculus

Pathways:

Acute Myeloid Leukemia, ASXL1 in AML

Identifier	Residue	Organism
SIGNOR-261288		Mus musculus
pmid	sentence
20660310	Beta-catenin/CBP-driven transcription is critical for maintenance of an undifferentiated/proliferative state

Publications:

1

Organism:

Mus Musculus

Tissue:

Lung

Pathways:

AMPK Signaling, COVID-19 Causal Network, FLT3-ITD signaling, Glioblastoma Multiforme, Malignant Melanoma, P38 Signaling, PI3K/AKT Signaling, SARS-CoV MAPK PERTURBATION, WNT Signaling

Identifier	Residue	Organism	Cell Line
SIGNOR-261216		Homo sapiens	Endothelial Progenitor Cell
pmid	sentence
29650961	Loss of ATP13A3 led to marked inhibition of serum-stimulated proliferation of BOECs, and increased apoptosis in serum-deprived conditions

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-241660		Mus musculus
pmid	sentence
26416890	The BAP1/ASXL2 Histone H2A Deubiquitinase Complex Regulates Cell Proliferation and is Disrupted in Cancer.

Publications:

1

Organism:

Mus Musculus

Identifier	Residue	Organism
SIGNOR-262533		Homo sapiens
pmid	sentence
21524151	Consistent with this, the magnitude of the response (i.e. the fraction of cells undergoing arrest) appears to diminish the closer the cells are to the time of S-phase entry. The existence of a time gap between full pRb phosphorylation and S-phase entry is also consistent with the notion that E2F, once released from pRb, transcriptionally activates factors needed for S-phase entry, a process which likely requires a significant amount of time.

Publications:

1

Organism:

Homo Sapiens

Pathways:

FLT3-ITD signaling, Luminal Breast Cancer, Malignant Melanoma, Pancreatic ductal adenocarcinoma (PDA), Rhabdomyosarcoma

Identifier	Residue	Organism
SIGNOR-277640		Homo sapiens
pmid	sentence
23075495	YAP and TAZ are two main downstream effectors of the Hippo pathway, and they function as transcription co-activators to promote cell proliferation and inhibit apoptosis.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-242138		Rattus norvegicus
pmid	sentence
17118269	However, evidence suggests that the detyrosination/tyrosination cycle of alpha-tubulin may be linked in some cell types to cell division and proliferationNF-Y

Publications:

1

Organism:

Rattus Norvegicus

Name	Proliferation
Primary ID	SIGNOR-PH4
Type	phenotype
Description	The multiplication or reproduction of cells, resulting in the expansion of a cell population
Relations	112
Pathways	Acute Myeloid Leukemia, AML1-ETO in AML, ASXL1 in AML, BCR-ABL in AML, DNMT3A in AML, FLT3 in AML, Onco-fusion proteins in AML, AML-IDH/TET, IDH-TET in AML, KIT in AML, miRNA in AML, MLL fusion protein in AML, NPM1 in AML, AML_TRIPLETS, AMPK Signaling, B-cell activation, COVID-19 Causal Network, Colorectal Carcinoma, EGFR Signaling, EBV infection, ErbB receptors in cancer, FLT3-ITD in AML, FLT3-ITD signaling, Glioblastoma Multiforme, Glucocorticoid receptor Signaling, Hippo in cancer, Hippo Signaling, Hepatocellular Tumor, iCAF signaling in PDAC, IL6 Signaling, Insulin Signaling, Integrin Signaling, Luminal Breast Cancer, Leptin Signaling, mTOR in cancer, Mitochondrial dynamics in T cell exhaustion, Malignant Melanoma, NF-KB Canonical, Triple mutant AML, NPM1_new, Non-small-cell lung cancer (NSCLC), P38 Signaling, Prostate Cancer, Pancreatic ductal adenocarcinoma (PDA), PPARgamma in cancer, PI3K/AKT Signaling, Retinoic acid Signaling, Rhabdomyosarcoma, RTKs in cancer, SARS-CoV MAPK PERTURBATION, TNF-alpha Signaling, Thyroid cancer, TGF-beta Signaling, TGFb in cancer, VEGF Signaling, Wnt in cancer, WNT Signaling, WNT/FLT3, YAP/TAZ regulation

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