Relation Results

Identifier	Residue	Organism
SIGNOR-199214		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-111680		Mus musculus
pmid	sentence
11907276	Caspase-3 cleaves parp-1. During cd95-mediated apoptosis proteolytic inactivation of parp-1 by caspases prevents atp depletion and thereby ensures the execution of the apoptotic process

Publications:

1

Organism:

Mus Musculus

Pathways:

Acute Myeloid Leukemia, COVID-19 Causal Network, Death Receptor Signaling, FLT3-ITD in AML, FLT3-ITD signaling, Inhibition of Apoptosis, Mitochondrial Control of Apoptosis, SARS-COV APOPTOSIS, TNF-alpha Signaling

Identifier	Residue	Organism
SIGNOR-261493		Homo sapiens
pmid	sentence
23567751	The mitochondrial pathway of apoptosis proceeds when the outer mitochondrial membrane (OMM) is compromised by the pro-apoptotic BCL-2 family members, BAK and BAX. Once activated, BAK and BAX form proteolipid pores in the OMM leading to mitochondrial outer membrane permeabilization (MOMP), and the release of inner membrane space proteins, such as cytochrome c, which promotes caspase activation.

Publications:

1

Organism:

Homo Sapiens

Pathways:

Acute Myeloid Leukemia, MLL fusion protein in AML, Malignant Melanoma

Identifier	Residue	Organism
SIGNOR-256582		Homo sapiens
pmid	sentence
26384349	Treatment with _-cyano-4-hydroxy cinnamate (CHC), a known inhibitor of MCT1, MCT2 and MCT4, dose-dependently induced cell death in MM cell lines and primary MM cells (Figure 1C). Thus, monocarboxylate transportation across membranes appears crucial for MM cell survival.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-256549		Homo sapiens
pmid	sentence
14585074	Downstream of caspase-8 activation, apoptosis induction takes place

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism	Cell Line
SIGNOR-249703		Homo sapiens	Neuron
pmid	sentence
20479780	The genetic causes of PD seem to participate in con verging pathways to pathogenesis, but it is unclear whether all or only some of these pathways need to be activated for lewy body deposition and neuronal death to occur.

Publications:

1

Organism:

Homo Sapiens

Pathways:

Parkinson

Identifier	Residue	Organism	Cell Line
SIGNOR-252939		Homo sapiens	HEK-293 Cell
pmid	sentence
14976264	Sirt1 inhibited foxo3's ability to induce cell death.

Publications:

1

Organism:

Homo Sapiens

Pathways:

Acute Myeloid Leukemia, BCR-ABL in AML, FLT3 in AML, FLT3-ITD in AML, FLT3-ITD signaling, NPM1_new

Identifier	Residue	Organism
SIGNOR-123218		Homo sapiens
pmid	sentence
15001576	Overexpression of traf7 induced caspase-dependent apoptosis.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism	Cell Line
SIGNOR-261243		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:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism	Cell Line
SIGNOR-256297		Homo sapiens	A-549 Cell
pmid	sentence
29928434	In addition, the downregulation of GSTA1 in A549 cells significantly induced cell apoptosis in vitro. In conclusion, GSTA1 plays an important role in regulation of cell proliferation and cell apoptosis in A549 cell line.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism	Cell Line
SIGNOR-264551		Homo sapiens	Fibroblast
pmid	sentence
19820693	We show that MeCP2 cooperates with HIPK2 in induction of apoptosis and that Ser 80 phosphorylation is required together with the DNA binding of MeCP2. \| We found increased cell death in each of the tested cell lines not only, as expected, when HIPK2 was overexpressed but also with MeCP2 alone. When both proteins were expressed together, the number of dead cells increased in an additive manner.

Publications:

1

Organism:

Homo Sapiens

Pathways:

Rett syndrome

Identifier	Residue	Organism	Cell Line
SIGNOR-251640		Homo sapiens	Alzheimer Disease Specific Cell Type
pmid	sentence
11578751	Alzheimer's disease, the cause of one of the most common types of dementia, is a brain disorder affecting the elderly and is characterized by the formation of two main protein aggregates: senile plaques and neurofibrillary tangles, which are involved in the process leading to progressive neuronal degeneration and death

Publications:

1

Organism:

Homo Sapiens

Pathways:

Alzheimer

Identifier	Residue	Organism	Cell Line
SIGNOR-260657		Homo sapiens	YTS-1 Cell
pmid	sentence
32164705	Our data showed that NEU1 inhibited cancer cell proliferation, induced apoptosis, and suppressed tumor formation both in vitro and in vivo, by disrupting interaction of FN and integrin β1 and inhibiting the Akt signaling pathway.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism	Cell Line
SIGNOR-256618		Mus musculus	Pro-B-lymphocyte
pmid	sentence
10082541	NFIL3 inhibits apoptosis without affecting Bcl-xL expression.

Publications:

1

Organism:

Mus Musculus

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-249615
pmid	sentence
10365962	Our results indicate that the Bcl-2 family of proteins bind to the VDAC in order to regulate the mitochondrial membrane potential and the release of cytochrome c during apoptosis.

Publications:

1

Identifier	Residue	Organism
SIGNOR-89244		Homo sapiens
pmid	sentence
14585074	Caspase-3 is responsible for apoptosis execution

Publications:

1

Organism:

Homo Sapiens

Pathways:

Alzheimer, COVID-19 Causal Network, Death Receptor Signaling, Inhibition of Apoptosis, Mitochondrial Control of Apoptosis, Parkinson, SARS-COV APOPTOSIS, TNF-alpha Signaling

Identifier	Residue	Organism	Cell Line
SIGNOR-251579		Homo sapiens	Neuron
pmid	sentence
25568892	Overexpression of AppBp1 in primary neurons induces apoptosis through the neddylation pathway

Publications:

1

Organism:

Homo Sapiens

Pathways:

Alzheimer

Identifier	Residue	Organism	Cell Line
SIGNOR-256263		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

Identifier	Residue	Organism	Cell Line
SIGNOR-256302		Homo sapiens	Umbilical Vein Endothelial Cell
pmid	sentence
21037234	In conclusion, AMPK stimulates HO-1 gene expression in human ECs via the Nrf2/antioxidant responsive element signaling pathway. The induction of HO-1 mediates the antiapoptotic effect of AMPK, and this may provide an important adaptive response to preserve EC viability during periods of metabolic stress.

Identifier	Residue	Organism	Cell Line
SIGNOR-256559		Homo sapiens	Breast Cancer Cell Line
pmid	sentence
26722274	Heme oxygenase-1 (HO-1) protects endothelial cells (EC) from undergoing apoptosis. These results indicated that HMOX-1 may be involved in conferring the chemoresistance of breast cancer cells, by preventing apoptosis and autophagy.

Publications:

2

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-260215		in vitro
pmid	sentence
14663477	Multiple studies supporting the role of Akt in apoptosis suppression have connected Akt to cell death regulation either by demonstrating its downregulation following pro-apoptotic insults, or by using gene-transfer experiments that transduce both activated, anti-apoptotic and inactive, pro-apoptotic mutants of Akt.

Publications:

1

Organism:

In Vitro

Pathways:

Acute Myeloid Leukemia, BCR-ABL in AML, FLT3 in AML, KIT in AML, miRNA in AML, AML_TRIPLETS, COVID-19 Causal Network, EBV infection, FLT3-ITD in AML, FLT3-ITD signaling, Inhibition of Apoptosis, Integrin Signaling, Malignant Melanoma, Triple mutant AML, NPM1_new, Pancreatic ductal adenocarcinoma (PDA), SARS-COV APOPTOSIS, Thyroid cancer

Identifier	Residue	Organism	Cell Line
SIGNOR-261686		Mus musculus	32D Cell
pmid	sentence
9710637	PLZF overexpression leads to apoptosis.

Publications:

1

Organism:

Mus Musculus

Pathways:

Acute Myeloid Leukemia, FLT3-ITD in AML

Identifier	Residue	Organism
SIGNOR-260178		Homo sapiens
pmid	sentence
18931691	JNKs activate apoptotic signaling by the upregulation pro-apoptotic genes via the transactivation of specific transcription factors or by directly modulating the activities of mitochondrial pro- and anti-apoptotic proteins through distinct phosphorylation events.

Publications:

1

Organism:

Homo Sapiens

Pathways:

COVID-19 Causal Network, EBV infection, FLT3-ITD signaling, SARS-CoV MAPK PERTURBATION, SARS-CoV ER STRESS

Identifier	Residue	Organism
SIGNOR-217884		Homo sapiens
pmid	sentence
14976264	Sirt1 inhibited foxo3's ability to induce cell death.

Publications:

1

Organism:

Homo Sapiens

Pathways:

Acute Myeloid Leukemia, FLT3-ITD in AML

Identifier	Residue	Organism
SIGNOR-260994		Homo sapiens
pmid	sentence
12377771	PSAP is an important regulator of apoptosis

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism	Cell Line
SIGNOR-256259		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, Inhibition of Apoptosis, Mitochondrial Control of Apoptosis, Malignant Melanoma, SARS-COV APOPTOSIS

Identifier	Residue	Organism
SIGNOR-115772		Homo sapiens
pmid	sentence
11888928	Plagl1 has been shown to prevent the proliferation of tumor cells by inducing cell cycle arrest and apoptosis

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism	Cell Line
SIGNOR-256583		Homo sapiens	Lymphoid Cell
pmid	sentence
14530308	Specific inhibition of Stat5a/b promotes apoptosis of IL-2-responsive primary and tumor-derived lymphoid cells

Publications:

1

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, FLT3-ITD in AML, FLT3-ITD signaling, Triple mutant AML

Identifier	Residue	Organism
SIGNOR-199208		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-261217		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	Cell Line
SIGNOR-260208		Homo sapiens	JURKAT Cell
pmid	sentence
16048439	Overexpression of SARS-CoV E protein in T-cells promoted apoptosis

Publications:

1

Organism:

Homo Sapiens

Pathways:

COVID-19 Causal Network, SARS-COV APOPTOSIS, SARS-CoV MAPK PERTURBATION, SARS-CoV ER STRESS

Identifier	Residue	Organism	Cell Line
SIGNOR-260206		Homo sapiens	HuH-7 Cell
pmid	sentence
17597455	Open Reading Frame 8a of the Human Severe Acute Respiratory Syndrome Coronavirus Not Only Promotes Viral Replication but Also Induces Apoptosis

Publications:

1

Organism:

Homo Sapiens

Pathways:

COVID-19 Causal Network, SARS-COV APOPTOSIS, SARS-CoV STRESS GRANULES

Identifier	Residue	Organism	Cell Line
SIGNOR-259150		Homo sapiens	U2-OS Cell
pmid	sentence
30403180	Cell apoptosis is an important event in cancer progression. Overexpression of RBM10 dramatically induced U2OS cell apoptosis compared with negative control cells.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism	Cell Line
SIGNOR-262208		Homo sapiens	HCT-116 Cell, SW-480 Cell
pmid	sentence
30998268	ANXA3 downregulation evidently increased the apoptosis of HCT116 (Figure 2C) and SW480 (Figure 2D) cells, and Ox‐induced cell apoptosis was further aggravated by ANXA3 suppression.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-259870		Homo sapiens
pmid	sentence
11175361	Ets1 and Ets2 seem to play opposing roles in apoptosis. While Ets1 seems to activate pro-apoptotic pathways, Ets2 seems to inhibit apoptosis

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism	Cell Line
SIGNOR-264255		Homo sapiens	Microglia
pmid	sentence
18626062	CD38 knockdown was found to increase apoptosis in normal microglia, but played a protective role in LPS-stimulated microglia and reduced proinflammatory cytokine secretion (Figure 1)

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism	Cell Line
SIGNOR-260219		Chlorocebus aethiops	Vero Cell
pmid	sentence
16310778	We demonstrated that the adenovirus-mediated over-expression of SARS-CoV spike (S) protein and its C-terminal domain (S2) induce apoptosis in Vero E6 cells in a time- and dosage-dependent manner

Publications:

1

Organism:

Chlorocebus Aethiops

Pathways:

COVID-19 Causal Network, SARS-COV APOPTOSIS, SARS-CoV FIBROSIS, SARS-CoV ER STRESS

Identifier	Residue	Organism	Cell Line
SIGNOR-260204		Chlorocebus aethiops	COS-1 Cell
pmid	sentence
15294014	In the present paper, we show that SARS-CoV N is capable of inducing apoptosis of COS-1 monkey kidney cells in the absence of growth factors by down-regulating ERK (extracellular-signal-regulated kinase), up-regulating JNK (c-Jun N-terminal kinase) and p38 MAPK (mitogen-activated protein kinase) pathways, and affecting their downstream effectors.

Identifier	Residue	Organism	Cell Line
SIGNOR-260205		Chlorocebus aethiops	COS-1 Cell
pmid	sentence
17453707	SARS-CoV Nucleocapsid Protein Induced Apoptosis of COS-1 Mediated by the Mitochondrial Pathway

Identifier	Residue	Organism	Cell Line
SIGNOR-260199		Homo sapiens	Lung Fibroblast Cell Line
pmid	sentence
16845612	Co-transfection of M and N enhances the induction of apoptosis by M or N alone, which also suggests that the structural proteins of SARS-CoV may play an important role not only in the process of invasion but also in the pathogenetic process in cells.

Publications:

3

Organism:

Chlorocebus Aethiops, Homo Sapiens

Pathways:

COVID-19 Causal Network, SARS-COV APOPTOSIS, SARS-CoV MAPK PERTURBATION, SARS-CoV FIBROSIS, SARS-CoV STRESS GRANULES

Identifier	Residue	Organism	Cell Line
SIGNOR-260198		Homo sapiens	Lung Fibroblast Cell Line
pmid	sentence
16845612	Co-transfection of M and N enhances the induction of apoptosis by M or N alone, which also suggests that the structural proteins of SARS-CoV may play an important role not only in the process of invasion but also in the pathogenetic process in cells.

Publications:

1

Organism:

Homo Sapiens

Pathways:

COVID-19 Causal Network, SARS-COV APOPTOSIS

Identifier	Residue	Organism
SIGNOR-260195		Chlorocebus aethiops
pmid	sentence
15958670	These results indicated that the 3a protein induced apoptosis in Vero E6 cells.

Publications:

1

Organism:

Chlorocebus Aethiops

Pathways:

COVID-19 Causal Network, SARS-COV APOPTOSIS, SARS-CoV MAPK PERTURBATION

Identifier	Residue	Organism
SIGNOR-260194		Chlorocebus aethiops
pmid	sentence
16965829	Over-expression of severe acute respiratory syndrome coronavirus 3b protein induces both apoptosis and necrosis in Vero E6 cells

Publications:

1

Organism:

Chlorocebus Aethiops

Pathways:

COVID-19 Causal Network, SARS-COV APOPTOSIS, SARS-CoV MAPK PERTURBATION, SARS-CoV STRESS GRANULES

Identifier	Residue	Organism
SIGNOR-260203		Chlorocebus aethiops
pmid	sentence
18708124	A SARS-CoV protein, ORF-6, induces caspase-3 mediated, ER stress and JNK-dependent apoptosis

Publications:

1

Organism:

Chlorocebus Aethiops

Pathways:

COVID-19 Causal Network, SARS-COV APOPTOSIS, SARS-CoV STRESS GRANULES

Identifier	Residue	Organism	Cell Line
SIGNOR-260197		Homo sapiens	A-549 Cell
pmid	sentence
15564512	7a induces apoptosis via a caspase-dependent pathway and in cell lines derived from different organs, including lung, kidney, and liver. \| The overexpression of HA-tagged 7a (7a-HA) induces apoptosis in 293T (human kidney epithelial) cells, as evidenced by an increase in caspase-3 protease activity, a hallmark of apoptosis, which is comparable to that caused by the overexpression of BAX, a proapoptotic member of the Bcl-2 family

Identifier	Residue	Organism	Cell Line
SIGNOR-260209		Chlorocebus aethiops	Vero Cell
pmid	sentence
17686858	Cells expressing the ORF7a or ORF7b protein undergo apoptosis.

Publications:

2

Organism:

Homo Sapiens, Chlorocebus Aethiops

Pathways:

COVID-19 Causal Network, SARS-COV APOPTOSIS, SARS-CoV MAPK PERTURBATION

Identifier	Residue	Organism	Cell Line
SIGNOR-260210		Chlorocebus aethiops	Vero Cell
pmid	sentence
17686858	Cells expressing the ORF7a or ORF7b protein undergo apoptosis.

Publications:

1

Organism:

Chlorocebus Aethiops

Pathways:

COVID-19 Causal Network, SARS-COV APOPTOSIS

Identifier	Residue	Organism
SIGNOR-255678		Homo sapiens
pmid	sentence
24212651	P53 is a nuclear transcription factor with a pro-apoptotic function

Publications:

1

Organism:

Homo Sapiens

Pathways:

Acute Myeloid Leukemia, AML1-ETO in AML, DNMT3A in AML, Onco-fusion proteins in AML, KIT in AML, miRNA in AML, NPM1 in AML, AML_TRIPLETS, Colorectal Carcinoma, EBV infection, FLT3-ITD in AML, FLT3-ITD signaling, Mitochondrial Control of Apoptosis, Malignant Melanoma, Triple mutant AML, NPM1_new, P38 Signaling, p53 in cancer, Pancreatic ductal adenocarcinoma (PDA)

Identifier	Residue	Organism
SIGNOR-249611		Homo sapiens
pmid	sentence
1286168	Bcl-2 functions to inhibit apoptosis in a variety of in vitro and in vivo experiments, suggesting interference with a central mechanism of apoptosis

Publications:

1

Organism:

Homo Sapiens

Pathways:

Alzheimer, Acute Myeloid Leukemia, BCR-ABL in AML, DNMT3A in AML, FLT3 in AML, KIT in AML, miRNA in AML, MLL fusion protein in AML, AML_TRIPLETS, COVID-19 Causal Network, Colorectal Carcinoma, Death Receptor Signaling, FLT3-ITD signaling, Inhibition of Apoptosis, Mitochondrial Control of Apoptosis, Malignant Melanoma, Triple mutant AML, NPM1_new, p53 in cancer, SARS-COV APOPTOSIS, SARS-CoV MAPK PERTURBATION

Identifier	Residue	Organism	Cell Line
SIGNOR-217887		Homo sapiens	HEK-293 Cell
pmid	sentence
14976264	Sirt1 inhibited foxo3's ability to induce cell death.

Publications:

1

Organism:

Homo Sapiens

Pathways:

FLT3 in AML, Inhibition of Apoptosis, Integrin Signaling, Thyroid cancer

Identifier	Residue	Organism	Cell Line
SIGNOR-255873		Homo sapiens	Hematopoietic Stem Cell
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-124320		Homo sapiens
pmid	sentence
15093545	The promyelocytic leukemia (pml) protein is a potent growth suppressor and proapototic factor

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism	Cell Line
SIGNOR-251934		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	Organism
SIGNOR-256370		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-256474		Homo sapiens
pmid	sentence
14585074	Caspase-3 is responsible for apoptosis execution

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism	Cell Line
SIGNOR-261729		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	Organism
SIGNOR-260232		Homo sapiens
pmid	sentence
32201502	AT2 receptor stimulation has been associated, for instance, with protection of the brain against ischemia [94]. In essence, AT2 receptors are linked to vasodilatation, release of nitric oxide, tissue development and remodeling, by stimulating apoptosis and inhibition of cell growth

Publications:

1

Organism:

Homo Sapiens

Pathways:

COVID-19 Causal Network, Fibrosis, SARS-CoV FIBROSIS

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-256575
pmid	sentence
16146838	The results of 2 microarray experiments demonstrated that the aberrant activation of STAT proteins by Flt3-ITDs resulted in the up-regulation of several STAT5-responsive genes, such as Pim-1, Pim-2, and members of the SOCS (suppressor of cytokine signaling) protein family. These results are particularly interesting because recent data point to an important role of Pim kinases in the antiapoptosis of hematopoietic cells.

Publications:

1

Identifier	Residue	Organism	Cell Line
SIGNOR-256267		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

Identifier	Residue	Organism
SIGNOR-205465		Homo sapiens
pmid	sentence
25300915	This study unraveled a novel function ofhmga2in induction of apoptosis in human primary cell lines

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-90612		Homo sapiens
pmid	sentence
14585074	Downstream of caspase-8 activation, apoptosis induction takes place

Publications:

1

Organism:

Homo Sapiens

Pathways:

Alzheimer, COVID-19 Causal Network, Death Receptor Signaling, Mitochondrial Control of Apoptosis, SARS-COV APOPTOSIS, TNF-alpha Signaling

Identifier	Residue	Organism	Cell Line
SIGNOR-262506		Homo sapiens	NCI-H1299 Cell
pmid	sentence
33188728	We present here data demonstrating that among all viral proteins, Nsp1 causes the most severe viability reduction in the cells of human lung origin. We found that introduction of Nsp1, but not other viral proteins, induced apoptosis in H1299 cells

Publications:

1

Organism:

Homo Sapiens

Pathways:

SARS-COV APOPTOSIS, SARS-CoV MAPK PERTURBATION, SARS-CoV STRESS GRANULES, SARS-CoV ER STRESS

Identifier	Residue	Organism
SIGNOR-261494		Homo sapiens
pmid	sentence
23567751	The mitochondrial pathway of apoptosis proceeds when the outer mitochondrial membrane (OMM) is compromised by the pro-apoptotic BCL-2 family members, BAK and BAX. Once activated, BAK and BAX form proteolipid pores in the OMM leading to mitochondrial outer membrane permeabilization (MOMP), and the release of inner membrane space proteins, such as cytochrome c, which promotes caspase activation.

Publications:

1

Organism:

Homo Sapiens

Pathways:

Alzheimer, Acute Myeloid Leukemia, MLL fusion protein in AML, COVID-19 Causal Network, Death Receptor Signaling, FLT3-ITD signaling, Inhibition of Apoptosis, Mitochondrial Control of Apoptosis, Malignant Melanoma, p53 in cancer, SARS-COV APOPTOSIS, TNF-alpha Signaling

Identifier	Residue	Organism
SIGNOR-120558		Homo sapiens
pmid	sentence
14699954	Neurotrophin binding to p75ntrhas also been shown to induce apoptosis

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism	Cell Line
SIGNOR-260137		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
SIGNOR-251641		Homo sapiens
pmid	sentence
11578751	Alzheimer's disease, the cause of one of the most common types of dementia, is a brain disorder affecting the elderly and is characterized by the formation of two main protein aggregates: senile plaques and neurofibrillary tangles, which are involved in the process leading to progressive neuronal degeneration and death

Publications:

1

Organism:

Homo Sapiens

Pathways:

Alzheimer

Identifier	Residue	Organism
SIGNOR-82463		Homo sapiens
pmid	sentence
11007801	Huntingtin interacting protein 1 induces apoptosis via a novel caspase-dependent death effector domain.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-260865		Homo sapiens
pmid	sentence
27920254	Stress granules (SGs) are large macromolecular aggregates that contain translation initiation complexes and mRNAs. Stress granule formation coincides with translational repression, and stress granules actively signal to mediate cell fate decisions by signaling to the translation apparatus to (i) maintain translational repression, (ii) mount various transcriptional responses, including innate immunity, and (iii) repress apoptosis.

Publications:

1

Organism:

Homo Sapiens

Pathways:

COVID-19 Causal Network, SARS-CoV STRESS GRANULES

Identifier	Residue	Organism	Cell Line
SIGNOR-235731		Mus musculus	C2C12 Cell, Myoblast, Myofibroblast
pmid	sentence
15851482	Mirk diminishes the extent of myoblast apoptosis during the differentiation process, at least in part by direct modulation of p21cip1 localization.

Publications:

1

Organism:

Mus Musculus

Tissue:

Muscle, Myotube

Identifier	Residue	Organism
SIGNOR-260171		Homo sapiens
pmid	sentence
31226023	ATF4 also induces another bZIP protein C/EBP-homologous protein (CHOP), which is responsible for triggering apoptosis in cells under prolonged ER stress. ATF4 and CHOP further induce growth arrest and DNA damage–inducible protein 34 (GADD34),a regulatory subunit of protein phosphatase 1 (PP1) that dephosphorylates eIF2α. This negative feedback mechanism enables protein synthesis to resume after resolution of ER stress.

Publications:

1

Organism:

Homo Sapiens

Pathways:

COVID-19 Causal Network, P38 Signaling, SARS-CoV MAPK PERTURBATION, SARS-CoV ER STRESS

Identifier	Residue	Organism
SIGNOR-256581		Homo sapiens
pmid	sentence
26384349	Treatment with _-cyano-4-hydroxy cinnamate (CHC), a known inhibitor of MCT1, MCT2 and MCT4, dose-dependently induced cell death in MM cell lines and primary MM cells (Figure 1C). Thus, monocarboxylate transportation across membranes appears crucial for MM cell survival.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-201034		Homo sapiens
pmid	sentence
23415677	Ectopic hlf expression inhibits apoptosis in murine and human cells, suggesting that hlf is regulating a conserved transcriptional program that inhibits cell death.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-255473		Homo sapiens
pmid	sentence
17700533	Like p53, its homolog p73 transactivates proapoptotic genes and induces cell death.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-256560		Mus musculus
pmid	sentence
12553907	In contrast, c-Jun is required for the survival of liver tumor cells. Reduced tumor formation strictly correlated with high apoptotic indices in c-Jun-deficient tumors, suggesting that increased apoptosis in c-Jun-deficient liver tumors is the primary cause for impaired tumorigenesis.

Publications:

1

Organism:

Mus Musculus

Pathways:

Acute Myeloid Leukemia, AML1-ETO in AML, TNF-alpha Signaling

Identifier	Residue	Organism	Cell Line
SIGNOR-261683		Mus musculus	FL5.12 Cell
pmid	sentence
9393856	Bcl-xL Expression Prevents Cytochrome c Redistribution and Subsequent Mitochondrial Depolarization during Apoptosis. Bcl-xL expression prevented both cytochrome c redistribution and mitochondrial membrane depolarization. In contrast, zVAD treatment could not prevent either cytochrome c redistribution or mitochondrial membrane depolarization in control transfectants withdrawn from IL-3. Thus, cytochrome c redistribution from mitochondria is an early apoptotic event that precedes mitochondrial membrane depolarization. Bcl-xL expression functions to inhibit both of these events. In at least some forms of cell death, the ability of Bcl-xL to regulate these mitochondrial events cannot be mimicked by caspase inhibition

Publications:

1

Organism:

Mus Musculus

Pathways:

Acute Myeloid Leukemia, KIT in AML, COVID-19 Causal Network, FLT3-ITD in AML, Mitochondrial Control of Apoptosis, Malignant Melanoma, SARS-COV APOPTOSIS

Identifier	Residue	Organism
SIGNOR-255693		Homo sapiens
pmid	sentence
22021368	Once genetic mutation of AML1 occurs in hematopoietic cells, aberrant activation of NF-κB signaling exerts antiapoptotic and proliferation-promoting effects via activation of BCL-XL or JUNB.

Publications:

1

Organism:

Homo Sapiens

Pathways:

Acute Myeloid Leukemia, miRNA in AML, COVID-19 Causal Network, EBV infection, Fibrosis, FLT3-ITD signaling, Inhibition of Apoptosis, Pancreatic ductal adenocarcinoma (PDA), SARS-CoV FIBROSIS, SARS-CoV STRESS GRANULES, TNF-alpha Signaling

Identifier	Residue	Organism	Cell Line
SIGNOR-261904		Homo sapiens	K-562 Cell
pmid	sentence
21821001	The aim of this study was to investigate the role of inducible galectin-3 in leukemic cells escape of apoptotic stimuli. Notably, inducible galectin-3, which stabilized the pro-survival Bcl-2 family proteins Mcl-1, Bcl-xL, and Bcl-2, was essential for anti-apoptosis.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-102019		Homo sapiens
pmid	sentence
12807881	Here we show that ectopic expression of rfp in human embryonic kidney 293 cells causes extensive apoptosis, as assessed by multiple criteria.

Publications:

1

Organism:

Homo Sapiens

Tissue:

Kidney

Identifier	Residue	Organism	Cell Line
SIGNOR-261042		Homo sapiens	HEK-293T Cell
pmid	sentence
31653868	Here, we characterize a microprotein called PIGBOS and reveal a role for a mitochondrial protein in UPR signaling. Together, these results showed that loss of PIGBOS increases cellular sensitivity to ER stress, which in turn increases apoptosis and links PIGBOS levels to the ability of cells to survive stress.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism	Cell Line
SIGNOR-259876		Mus musculus	RGC-5 Cell
pmid	sentence
22194658	SiRNA effectively downregulated optineurin expression in RGC-5 and PC12 stable transfected cells. Optineurin siRNA significantly inhibited cell growth and increased apoptosis in RGC-5 and PC12 cells. Microarray analysis identified 112 differentially expressed genes in optineurin siRNA transfected RGC-5 cells. Quantitative real-time PCR and western blot confirmed that the expression of brain-derived neurotrophic factor (Bdnf), neurotrophin-3(Ntf3), synaptosomal-associated protein 25(Snap25), and neurofilament, light polypeptide(Nefl) was significantly downregulated in RGC-5 and PC12 cells transfected with optineurin siRNA.

Publications:

1

Organism:

Mus Musculus

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-249623
pmid	sentence
16146838	The results of 2 microarray experiments demonstrated that the aberrant activation of STAT proteins by Flt3-ITDs resulted in the up-regulation of several STAT5-responsive genes, such as Pim-1, Pim-2, and members of the SOCS (suppressor of cytokine signaling) protein family. These results are particularly interesting because recent data point to an important role of Pim kinases in the antiapoptosis of hematopoietic cells.

Publications:

1

Pathways:

Acute Myeloid Leukemia, FLT3 in AML, FLT3-ITD in AML, FLT3-ITD signaling

Identifier	Residue	Organism	Cell Line
SIGNOR-261689		Homo sapiens	Kasumi-1 Cell
pmid	sentence
17464329	We next focused on the pro-apoptotic function of ANXA1 in AML1-ETO-expressing AML cells. In this regard, FK228 was found to increase the protein levels of both the full-length and 33 kDa N-terminal cleavage products of ANXA1, which led to the localization of ANXA1 on the plasma membrane. Conversely, the inhibition of ANXA1 function (by ANXA1 neutralizing antibody, which blocked ANXA1 localization on the plasma membrane) or expression (by siRNA) significantly reduced FK228-induced apoptosis, indicating that ANXA1 is involved in apoptosis induction in response to FK228.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-264545		Mus musculus
pmid	sentence
26344767	To further determine whether MeCP2 regulates the expression of miR-199a, we also re-expressed MeCP2 in MeCP2-KO neurons. As expected, this restored the level of mature-miR-199a expression to that in WT neurons

Publications:

1

Organism:

Mus Musculus

Pathways:

Rett syndrome

Identifier	Residue	Organism
SIGNOR-140391		Homo sapiens
pmid	sentence
16153597	We observed that foxl2 induces apoptosis in the ovarian cells unveiling a novel function of foxl2

Publications:

1

Organism:

Homo Sapiens

Tissue:

Ovary

Identifier	Residue	Organism	Cell Line
SIGNOR-260426		Homo sapiens	HEP-3B Cell
pmid	sentence
17960585	Transforming growth factor-beta (TGF-beta) signaling is known to depend on the formation of Smad2/3-Smad4 transcription regulatory complexes. Functional analysis revealed that Smad3 and Smad4 were the predominant mediators of TGF-beta-induced apoptosis in Hep3B cells. We provide evidence that up-regulation of Bcl-2-interacting mediator of cell death (Bim), under the transcriptional control of Smad3-Smad4 signaling, is crucial to TGF-beta-induced apoptosis in Hep3B cells.

Publications:

1

Organism:

Homo Sapiens

Pathways:

COVID-19 Causal Network, Fibrosis, Inhibition of Apoptosis, Mitochondrial Control of Apoptosis, SARS-COV APOPTOSIS, SARS-CoV FIBROSIS

Identifier	Residue	Organism
SIGNOR-259869		Homo sapiens
pmid	sentence
11175361	Ets1 and Ets2 seem to play opposing roles in apoptosis. While Ets1 seems to activate pro-apoptotic pathways, Ets2 seems to inhibit apoptosis

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism	Cell Line
SIGNOR-255732		Homo sapiens	Hematopoietic Cell
pmid	sentence
16146838	The results of 2 microarray experiments demonstrated that the aberrant activation of STAT proteins by Flt3-ITDs resulted in the up-regulation of several STAT5-responsive genes, such as Pim-1, Pim-2, and members of the SOCS (suppressor of cytokine signaling) protein family. These results are particularly interesting because recent data point to an important role of Pim kinases in the antiapoptosis of hematopoietic cells.

Publications:

1

Organism:

Homo Sapiens

Pathways:

Acute Myeloid Leukemia, FLT3 in AML, FLT3-ITD in AML

Identifier	Residue	Organism
SIGNOR-266855		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
SIGNOR-259398		Homo sapiens
pmid	sentence
30455429	Over-expression of NR4A3 attenuated proliferation of cancer cells and promoted apoptosis by augmenting the expression of pro-apoptotic genes, PUMA and Bax.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-261365		Homo sapiens
pmid	sentence
18034316	a pro-apoptotic member of the QSOX superfamily, QSOXN, was described (Wittke et al. 2003). QSOXN was shown to sensitize neuroblastoma cells to INFγ-induced apoptosis, by still unknown mechanisms. In this context, absence of QSOX in fetal epithelia may prevent apoptosis.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism	Cell Line
SIGNOR-264550		Homo sapiens	Fibroblast
pmid	sentence
19820693	We show that MeCP2 cooperates with HIPK2 in induction of apoptosis and that Ser 80 phosphorylation is required together with the DNA binding of MeCP2. \| We found increased cell death in each of the tested cell lines not only, as expected, when HIPK2 was overexpressed but also with MeCP2 alone. When both proteins were expressed together, the number of dead cells increased in an additive manner.

Publications:

1

Organism:

Homo Sapiens

Pathways:

Acute Myeloid Leukemia, miRNA in AML, Rett syndrome

Identifier	Residue	Organism	Cell Line
SIGNOR-271556		Homo sapiens	HEK-293 Cell
pmid	sentence
16522193	MEX can act as an E3, Ub (ubiquitin) ligase, through the E2, Ub-conjugating enzymes UbcH5a, UbcH5c or UbcH6. A region of MEX that contains the RING fingers and the ZZ zinc finger was required for interaction with UbcH5a and MEX self-association, whereas the SWIM domain was critical for MEX ubiquitination. The expression of MEX promoted apoptosis that was induced through Fas, DR (death receptor) 3 and DR4 signalling, but not that mediated by the BH3 (Bcl-2 homology 3)-only protein BimEL or the chemotherapeutic drug adriamycin.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism	Cell Line
SIGNOR-255860		Homo sapiens	Leukemia Cell
pmid	sentence
19109563	To discern the mechanisms by which Meis1 inhibition leads to reduced cell growth, we performed cell-cycle and apoptosis analyses.Meis1 knockdown also resulted in increased apoptosis, as evidenced by increased uptake of PI and a stain for activated caspases (CaspaTag) by M26-transduced cells compared with control cells. These results indicate that Meis1 is required for proliferation and survival of 4166 leukemia cells.

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	Cell Line
SIGNOR-261809		Homo sapiens	EB-1 Cell
pmid	sentence
12135761	The PRG3 gene is a potential p53 target gene in a p53‐dependent apoptosis pathway. These results clearly indicate that the ectopic expression of PRG3 induces apoptosis.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-183153		Homo sapiens
pmid	sentence
19127412	Overexpression of foxa1 promoted apoptosis

Publications:

1

Organism:

Homo Sapiens

Name	Apoptosis
Primary ID	SIGNOR-PH2
Type	phenotype
Description	The process of programmed cell death
Relations	95
Pathways	Alzheimer, Acute Myeloid Leukemia, BCR-ABL in AML, DNMT3A in AML, FLT3 in AML, Onco-fusion proteins in AML, KIT in AML, miRNA in AML, MLL fusion protein in AML, NPM1 in AML, AML_TRIPLETS, COVID-19 Causal Network, Colorectal Carcinoma, Death Receptor Signaling, EBV infection, Fibrosis, FLT3-ITD in AML, FLT3-ITD signaling, Hippo in cancer, Hippo Signaling, Inhibition of Apoptosis, Integrin Signaling, Mitochondrial Control of Apoptosis, Malignant Melanoma, Triple mutant AML, NPM1_new, P38 Signaling, p53 in cancer, Parkinson, Pancreatic ductal adenocarcinoma (PDA), Rett syndrome, SARS-COV APOPTOSIS, SARS-CoV MAPK PERTURBATION, SARS-CoV FIBROSIS, SARS-CoV STRESS GRANULES, SARS-CoV ER STRESS, TNF-alpha Signaling, Thyroid cancer

The SIGnaling Network
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