+ |
PRKCA | up-regulates quantity by stabilization
phosphorylation
|
TWIST1 |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-277429 |
Ser144 |
TLPSDKLsKIQTLKL |
Homo sapiens |
HEK-293T Cell |
pmid |
sentence |
30733340 |
Because most of these sites were predicted to be phosphorylated by protein kinase C (PKC), we overexpressed PKCα in several cell lines and found that it phosphorylates Twist1 on Ser-144. we observed that PKCα-mediated Twist1 phosphorylation at Ser-144 inhibits Twist1 ubiquitination and consequently stabilizes it. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
CSNK2A1 | up-regulates
phosphorylation
|
TWIST1 |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-173668 |
Ser18 |
SPADDSLsNSEEEPD |
Homo sapiens |
|
pmid |
sentence |
21559372 |
Further investigation revealed that il-6 stabilizes twist in scchn cell lines through casein kinase 2 (ck2) phosphorylation of twist residues s18 and s20, and that this phosphorylation inhibits degradation of twist. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-173672 |
Ser20 |
ADDSLSNsEEEPDRQ |
Homo sapiens |
|
pmid |
sentence |
21559372 |
Further investigation revealed that il-6 stabilizes twist in scchn cell lines through casein kinase 2 (ck2) phosphorylation of twist residues s18 and s20, and that this phosphorylation inhibits degradation of twist. |
|
Publications: |
2 |
Organism: |
Homo Sapiens |
+ |
AKT | up-regulates
phosphorylation
|
TWIST1 |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-244373 |
Ser42 |
GGRKRRSsRRSAGGG |
Homo sapiens |
|
pmid |
sentence |
20400976 |
Moreover, phosphorylation of twist-1 at ser42 was shown in vivo in various human cancer tissues, suggesting that this post-translational modification ensures functional activation of twist-1 after promotion of survival during carcinogenesis. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Acute Myeloid Leukemia, miRNA in AML |
+ |
AKT1 | up-regulates
phosphorylation
|
TWIST1 |
0.451 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-164884 |
Ser42 |
GGRKRRSsRRSAGGG |
Homo sapiens |
|
pmid |
sentence |
20400976 |
Moreover, phosphorylation of twist-1 at ser42 was shown in vivo in various human cancer tissues, suggesting that this post-translational modification ensures functional activation of twist-1 after promotion of survival during carcinogenesis. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
MAPK1 | up-regulates
phosphorylation
|
TWIST1 |
0.31 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-173401 |
Ser68 |
GGGDEPGsPAQGKRG |
Homo sapiens |
HEK-293 Cell, Breast Cancer Cell |
pmid |
sentence |
21502402 |
We identified the serine 68 (s68) as a major phosphorylation site of twist1 by mass spectrometry and with specific antibodies. This s68 is phosphorylated by p38, jnk and erk1/2 in vitro, and its phosphorylation levels positively correlate with twist1 protein levels in hek293 and breast cancer cells. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
CTDSP1 | down-regulates activity
dephosphorylation
|
TWIST1 |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-245962 |
Ser68 |
GGGDEPGsPAQGKRG |
Homo sapiens |
HEK-293 Cell |
pmid |
sentence |
26975371 |
These results indicate that SCP1 is the phosphatase that counter-regulates the MAPK-mediated phosphorylation of S68-Twist1. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
MAPK14 | up-regulates
phosphorylation
|
TWIST1 |
0.273 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-173409 |
Ser68 |
GGGDEPGsPAQGKRG |
Homo sapiens |
Breast Cancer Cell |
pmid |
sentence |
21502402 |
Phosphorylation of serine 68 of twist1 by mapks stabilizes twist1 protein and promotes breast cancer cell invasiveness. this ser 68 is phosphorylated by p38, c-jun n-terminal kinases (jnk), and extracellular signal-regulated kinases1/2 in vitro |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
MAPK3 | up-regulates
phosphorylation
|
TWIST1 |
0.335 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-173413 |
Ser68 |
GGGDEPGsPAQGKRG |
Homo sapiens |
Breast Cancer Cell |
pmid |
sentence |
21502402 |
Phosphorylation of serine 68 of twist1 by mapks stabilizes twist1 protein and promotes breast cancer cell invasiveness. this ser 68 is phosphorylated by p38, c-jun n-terminal kinases (jnk), and extracellular signal-regulated kinases1/2 in vitro |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
MAPK8 | up-regulates
phosphorylation
|
TWIST1 |
0.314 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-173417 |
Ser68 |
GGGDEPGsPAQGKRG |
Homo sapiens |
Breast Cancer Cell |
pmid |
sentence |
21502402 |
Phosphorylation of serine 68 of twist1 by mapks stabilizes twist1 protein and promotes breast cancer cell invasiveness. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Acute Myeloid Leukemia |
+ |
MAPK11 | up-regulates
phosphorylation
|
TWIST1 |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-173405 |
Ser68 |
GGGDEPGsPAQGKRG |
Homo sapiens |
Breast Cancer Cell |
pmid |
sentence |
21502402 |
Phosphorylation of serine 68 of twist1 by mapks stabilizes twist1 protein and promotes breast cancer cell invasiveness. this ser 68 is phosphorylated by p38, c-jun n-terminal kinases (jnk), and extracellular signal-regulated kinases1/2 in vitro |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
TWIST1 | down-regulates quantity by repression
transcriptional regulation
|
RBL2 |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255535 |
|
|
Homo sapiens |
HGC-27 Cell |
pmid |
sentence |
19051271 |
we performed microarray analysis to compare the gene expression profiles in HGC-27 cells, with or without small interfering RNA (siRNA)-mediated depletion of TWIST. Our results showed that NF1, RAP1A, SRPX, RBL2, PFDN4, ILK, F2R, ERBB3, and MYB were up-regulated, whereas AKR1C2, FOS, GDF15, NR2F1, ATM, and CTPS were down-regulated after TWIST depletion |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
TWIST1 | up-regulates quantity by expression
transcriptional regulation
|
SNAI2 |
0.49 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255524 |
|
|
Homo sapiens |
|
pmid |
sentence |
20646316 |
Individual genes upregulated by TWIST1 known to promote EMT and/or GBM invasion included SNAI2, MMP2, HGF, FAP and FN1. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
TWIST1 | up-regulates quantity by expression
transcriptional regulation
|
ITGB1 |
0.296 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255516 |
|
|
Homo sapiens |
HEY Cell |
pmid |
sentence |
17487558 |
Immunoblot analysis showed that HEY/si-TWIST cells exhibited decreased expression levels of CD29, CD44 and CD54 compared to those of HEY/si-scrambled cells |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
TWIST1 | down-regulates quantity by repression
transcriptional regulation
|
CDH1 |
0.498 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255157 |
|
|
Homo sapiens |
|
pmid |
sentence |
15311212 |
known E-cadherin transcriptional repressors, such as SLUG (SNAI2), SIP1 (ZEB2), TWIST1, SNAIL (SNAI1) and ZEB1 (TCF8), but not E12/E47 (TCF3), had a lack of upregulation in cells expressing mutated E-cadherin compared to WT. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
SUZ12 | down-regulates quantity by repression
transcriptional regulation
|
TWIST1 |
0.282 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-254155 |
|
|
Homo sapiens |
MCF-10A Cell |
pmid |
sentence |
23836662 |
We further demonstrated that PER2 served as a transcriptional corepressor, which recruited polycomb proteins EZH2 and SUZ12 as well as HDAC2 to octamer transcription factor 1 (OCT1) (POU2F1) binding sites of the TWIST1 and SLUG promoters to repress expression of these EMT genes. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
HDAC2 | down-regulates quantity by repression
transcriptional regulation
|
TWIST1 |
0.389 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-254154 |
|
|
Homo sapiens |
MCF-10A Cell |
pmid |
sentence |
23836662 |
We further demonstrated that PER2 served as a transcriptional corepressor, which recruited polycomb proteins EZH2 and SUZ12 as well as HDAC2 to octamer transcription factor 1 (OCT1) (POU2F1) binding sites of the TWIST1 and SLUG promoters to repress expression of these EMT genes. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
TWIST1 | up-regulates quantity by expression
transcriptional regulation
|
FOS |
0.494 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255526 |
|
|
Homo sapiens |
HGC-27 Cell |
pmid |
sentence |
19051271 |
we performed microarray analysis to compare the gene expression profiles in HGC-27 cells, with or without small interfering RNA (siRNA)-mediated depletion of TWIST. Our results showed that NF1, RAP1A, SRPX, RBL2, PFDN4, ILK, F2R, ERBB3, and MYB were up-regulated, whereas AKR1C2, FOS, GDF15, NR2F1, ATM, and CTPS were down-regulated after TWIST depletion |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Acute Myeloid Leukemia, miRNA in AML |
+ |
TWIST1 | down-regulates quantity by repression
transcriptional regulation
|
ILK |
0.286 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255528 |
|
|
Homo sapiens |
HGC-27 Cell |
pmid |
sentence |
19051271 |
we performed microarray analysis to compare the gene expression profiles in HGC-27 cells, with or without small interfering RNA (siRNA)-mediated depletion of TWIST. Our results showed that NF1, RAP1A, SRPX, RBL2, PFDN4, ILK, F2R, ERBB3, and MYB were up-regulated, whereas AKR1C2, FOS, GDF15, NR2F1, ATM, and CTPS were down-regulated after TWIST depletion |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
FBXO45 | down-regulates quantity by destabilization
binding
|
TWIST1 |
0.263 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-272183 |
|
|
Homo sapiens |
HEK-293 Cell |
pmid |
sentence |
25460509 |
One of the hallmarks of EMT is loss of E-cadherin and gain of N-cadherin expression, which are regulated by the core EMT-inducing transcription factors (EMT-TFs), such as Zeb1/2, Snai1/2 and Twist1. Here, we find that EMT-TFs can be dynamically degraded by an atypical ubiquitin E3 ligase complex Skp1-Pam-Fbxo45 (SPFFbxo45) through the ubiquitin proteasome system (UPS). The key step is recognition of EMT-TFs by Fbxo45 through its SPRY domain for Zeb2, or F-box domain for the other three EMT-TFs Snai1, Snai2 and Twist1, respectively. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
TWIST1 | up-regulates quantity by expression
transcriptional regulation
|
FN1 |
0.422 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255521 |
|
|
Homo sapiens |
GBM-8401 Cell |
pmid |
sentence |
20646316 |
Individual genes upregulated by TWIST1 known to promote EMT and/or GBM invasion included SNAI2, MMP2, HGF, FAP and FN1. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
TWIST1 | up-regulates quantity by expression
transcriptional regulation
|
ATM |
0.294 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255511 |
|
|
Homo sapiens |
HGC-27 Cell |
pmid |
sentence |
19051271 |
we performed microarray analysis to compare the gene expression profiles in HGC-27 cells, with or without small interfering RNA (siRNA)-mediated depletion of TWIST. Our results showed that NF1, RAP1A, SRPX, RBL2, PFDN4, ILK, F2R, ERBB3, and MYB were up-regulated, whereas AKR1C2, FOS, GDF15, NR2F1, ATM, and CTPS were down-regulated after TWIST depletion |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
TWIST1 | down-regulates quantity by repression
transcriptional regulation
|
PFDN4 |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255532 |
|
|
Homo sapiens |
HGC-27 Cell |
pmid |
sentence |
19051271 |
we performed microarray analysis to compare the gene expression profiles in HGC-27 cells, with or without small interfering RNA (siRNA)-mediated depletion of TWIST. Our results showed that NF1, RAP1A, SRPX, RBL2, PFDN4, ILK, F2R, ERBB3, and MYB were up-regulated, whereas AKR1C2, FOS, GDF15, NR2F1, ATM, and CTPS were down-regulated after TWIST depletion |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
TWIST1 | up-regulates quantity by expression
transcriptional regulation
|
GDF15 |
0.282 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255527 |
|
|
Homo sapiens |
HGC-27 Cell |
pmid |
sentence |
19051271 |
we performed microarray analysis to compare the gene expression profiles in HGC-27 cells, with or without small interfering RNA (siRNA)-mediated depletion of TWIST. Our results showed that NF1, RAP1A, SRPX, RBL2, PFDN4, ILK, F2R, ERBB3, and MYB were up-regulated, whereas AKR1C2, FOS, GDF15, NR2F1, ATM, and CTPS were down-regulated after TWIST depletion |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
Skp1-Pam E3 | down-regulates quantity by destabilization
polyubiquitination
|
TWIST1 |
0.253 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-272190 |
|
|
Homo sapiens |
HEK-293 Cell |
pmid |
sentence |
25460509 |
One of the hallmarks of EMT is loss of E-cadherin and gain of N-cadherin expression, which are regulated by the core EMT-inducing transcription factors (EMT-TFs), such as Zeb1/2, Snai1/2 and Twist1. Here, we find that EMT-TFs can be dynamically degraded by an atypical ubiquitin E3 ligase complex Skp1-Pam-Fbxo45 (SPFFbxo45) through the ubiquitin proteasome system (UPS). The key step is recognition of EMT-TFs by Fbxo45 through its SPRY domain for Zeb2, or F-box domain for the other three EMT-TFs Snai1, Snai2 and Twist1, respectively. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
ZRANB1 | down-regulates activity
deubiquitination
|
TWIST1 |
0.338 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-273502 |
|
|
Homo sapiens |
HEK-293 Cell |
pmid |
sentence |
29748601 |
Trabid inhibits Twist1 activity by cleaving RNF8-mediated Twist1 K63-linked ubiquitination |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
TWIST1 | up-regulates quantity by expression
transcriptional regulation
|
HGF |
0.332 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255522 |
|
|
Homo sapiens |
GBM-8401 Cell |
pmid |
sentence |
20646316 |
Individual genes upregulated by TWIST1 known to promote EMT and/or GBM invasion included SNAI2, MMP2, HGF, FAP and FN1. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
TWIST1 | down-regulates
|
CSNK2A1 |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-192064 |
|
|
Homo sapiens |
|
pmid |
sentence |
22975381 |
Ck2-mediated phosphorylation at ser392 of p53 was attenuated in the presence of recombinant twist1 |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
TWIST1 | down-regulates quantity by repression
transcriptional regulation
|
RAP1A |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255533 |
|
|
Homo sapiens |
HGC-27 Cell |
pmid |
sentence |
19051271 |
we performed microarray analysis to compare the gene expression profiles in HGC-27 cells, with or without small interfering RNA (siRNA)-mediated depletion of TWIST. Our results showed that NF1, RAP1A, SRPX, RBL2, PFDN4, ILK, F2R, ERBB3, and MYB were up-regulated, whereas AKR1C2, FOS, GDF15, NR2F1, ATM, and CTPS were down-regulated after TWIST depletion |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
ERK1/2 | up-regulates
phosphorylation
|
TWIST1 |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-270209 |
|
|
Homo sapiens |
Breast Cancer Cell |
pmid |
sentence |
21502402 |
Phosphorylation of serine 68 of twist1 by mapks stabilizes twist1 protein and promotes breast cancer cell invasiveness. this ser 68 is phosphorylated by p38, c-jun n-terminal kinases (jnk), and extracellular signal-regulated kinases1/2 in vitro |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Acute Myeloid Leukemia |
+ |
TWIST1 | up-regulates quantity by expression
transcriptional regulation
|
NR2F1 |
0.253 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255531 |
|
|
Homo sapiens |
HGC-27 Cell |
pmid |
sentence |
19051271 |
we performed microarray analysis to compare the gene expression profiles in HGC-27 cells, with or without small interfering RNA (siRNA)-mediated depletion of TWIST. Our results showed that NF1, RAP1A, SRPX, RBL2, PFDN4, ILK, F2R, ERBB3, and MYB were up-regulated, whereas AKR1C2, FOS, GDF15, NR2F1, ATM, and CTPS were down-regulated after TWIST depletion |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
TWIST1 | down-regulates quantity by repression
transcriptional regulation
|
MYB |
0.249 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255529 |
|
|
Homo sapiens |
HGC-27 Cell |
pmid |
sentence |
19051271 |
we performed microarray analysis to compare the gene expression profiles in HGC-27 cells, with or without small interfering RNA (siRNA)-mediated depletion of TWIST. Our results showed that NF1, RAP1A, SRPX, RBL2, PFDN4, ILK, F2R, ERBB3, and MYB were up-regulated, whereas AKR1C2, FOS, GDF15, NR2F1, ATM, and CTPS were down-regulated after TWIST depletion |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
EZH2 | down-regulates quantity by repression
transcriptional regulation
|
TWIST1 |
0.337 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-254151 |
|
|
Homo sapiens |
MCF-10A Cell |
pmid |
sentence |
23836662 |
We further demonstrated that PER2 served as a transcriptional corepressor, which recruited polycomb proteins EZH2 and SUZ12 as well as HDAC2 to octamer transcription factor 1 (OCT1) (POU2F1) binding sites of the TWIST1 and SLUG promoters to repress expression of these EMT genes. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Acute Myeloid Leukemia |
+ |
POU2F1 | up-regulates quantity by expression
transcriptional regulation
|
TWIST1 |
0.26 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-254152 |
|
|
Homo sapiens |
MCF-10A Cell |
pmid |
sentence |
23836662 |
This PER2-OCT1 interaction effectively converted OCT1 sites, which normally activate expression, into repressor sites by recruitment of a polycomb repressor complex including EZH2 and SUZ12, as well as HDAC2. We further demonstrated that PER2 served as a transcriptional corepressor, which recruited polycomb proteins EZH2 and SUZ12 as well as HDAC2 to octamer transcription factor 1 (OCT1) (POU2F1) binding sites of the TWIST1 and SLUG promoters to repress expression of these EMT genes. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
PER2 | down-regulates quantity by repression
transcriptional regulation
|
TWIST1 |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-254153 |
|
|
Homo sapiens |
MCF-10A Cell |
pmid |
sentence |
23836662 |
We further demonstrated that PER2 served as a transcriptional corepressor, which recruited polycomb proteins EZH2 and SUZ12 as well as HDAC2 to octamer transcription factor 1 (OCT1) (POU2F1) binding sites of the TWIST1 and SLUG promoters to repress expression of these EMT genes. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
TWIST1 | down-regulates quantity by repression
transcriptional regulation
|
RUNX2 |
0.461 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255593 |
|
|
Homo sapiens |
Mesenchymal Stem Cell |
pmid |
sentence |
21931630 |
Using human MSCs, we discovered TWIST, a downstream target of HIF-1α, was induced under hypoxia and acted as a transcription repressor of RUNX2 through binding to the E-box located on the promoter of type 1 RUNX2. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
TWIST1 | up-regulates quantity by expression
transcriptional regulation
|
FAP |
0.244 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255523 |
|
|
Homo sapiens |
|
pmid |
sentence |
20646316 |
Individual genes upregulated by TWIST1 known to promote EMT and/or GBM invasion included SNAI2, MMP2, HGF, FAP and FN1. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
RUNX2 | up-regulates quantity by expression
transcriptional regulation
|
TWIST1 |
0.461 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255085 |
|
|
Homo sapiens |
Thyroid Cancer Cell Line |
pmid |
sentence |
22641097 |
Effective silencing of Runx2 by short interfering RNA (siRNA) demonstrated downregulation of EMT-related molecules (SNAI2, SNAI3 and TWIST1), MMP2 and vasculogenic factors (VEGFA and VEGFC) in thyroid carcinoma cells. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
Gbeta | up-regulates
phosphorylation
|
TWIST1 |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-270122 |
|
|
Homo sapiens |
Breast Cancer Cell |
pmid |
sentence |
21502402 |
Phosphorylation of serine 68 of twist1 by mapks stabilizes twist1 protein and promotes breast cancer cell invasiveness. this ser 68 is phosphorylated by p38, c-jun n-terminal kinases (jnk), and extracellular signal-regulated kinases1/2 in vitro |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
TWIST1 | down-regulates quantity by repression
transcriptional regulation
|
SRPX |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255534 |
|
|
Homo sapiens |
HGC-27 Cell |
pmid |
sentence |
19051271 |
we performed microarray analysis to compare the gene expression profiles in HGC-27 cells, with or without small interfering RNA (siRNA)-mediated depletion of TWIST. Our results showed that NF1, RAP1A, SRPX, RBL2, PFDN4, ILK, F2R, ERBB3, and MYB were up-regulated, whereas AKR1C2, FOS, GDF15, NR2F1, ATM, and CTPS were down-regulated after TWIST depletion |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
TWIST1 | up-regulates quantity by expression
transcriptional regulation
|
CTPS1 |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255518 |
|
|
Homo sapiens |
HGC-27 Cell |
pmid |
sentence |
19051271 |
we performed microarray analysis to compare the gene expression profiles in HGC-27 cells, with or without small interfering RNA (siRNA)-mediated depletion of TWIST. Our results showed that NF1, RAP1A, SRPX, RBL2, PFDN4, ILK, F2R, ERBB3, and MYB were up-regulated, whereas AKR1C2, FOS, GDF15, NR2F1, ATM, and CTPS were down-regulated after TWIST depletion |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
TWIST1 | up-regulates quantity by expression
transcriptional regulation
|
ICAM1 |
0.268 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255515 |
|
|
Homo sapiens |
HEY Cell |
pmid |
sentence |
17487558 |
Immunoblot analysis showed that HEY/si-TWIST cells exhibited decreased expression levels of CD29, CD44 and CD54 compared to those of HEY/si-scrambled cells |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
TWIST1 | up-regulates quantity by expression
transcriptional regulation
|
MMP2 |
0.385 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255525 |
|
|
Homo sapiens |
GBM-8401 Cell |
pmid |
sentence |
20646316 |
Individual genes upregulated by TWIST1 known to promote EMT and/or GBM invasion included SNAI2, MMP2, HGF, FAP and FN1. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
TWIST1 | down-regulates quantity by repression
transcriptional regulation
|
F2R |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255520 |
|
|
Homo sapiens |
HGC-27 Cell |
pmid |
sentence |
19051271 |
we performed microarray analysis to compare the gene expression profiles in HGC-27 cells, with or without small interfering RNA (siRNA)-mediated depletion of TWIST. Our results showed that NF1, RAP1A, SRPX, RBL2, PFDN4, ILK, F2R, ERBB3, and MYB were up-regulated, whereas AKR1C2, FOS, GDF15, NR2F1, ATM, and CTPS were down-regulated after TWIST depletion |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
TWIST1 | up-regulates quantity by expression
transcriptional regulation
|
mir-10b |
0.4 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255887 |
|
|
Homo sapiens |
|
pmid |
sentence |
23132946 |
We then showed that ectopic expression of MLL fusion genes in both human and mouse normal hematopoietic stem/progenitor cells could significantly down-regulate endogenous expression of miR-495 and that the depletion of MLL fusions resulted in the up-regulation of miR-495. Thus, our data suggest that there is an MLL-fusion–mediated negative regulation of the production of miR-495 in hematopoietic cells. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Acute Myeloid Leukemia, miRNA in AML |
+ |
TWIST1 | up-regulates quantity by expression
transcriptional regulation
|
AKR1C2 |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255510 |
|
|
Homo sapiens |
HGC-27 Cell |
pmid |
sentence |
19051271 |
we performed microarray analysis to compare the gene expression profiles in HGC-27 cells, with or without small interfering RNA (siRNA)-mediated depletion of TWIST. Our results showed that NF1, RAP1A, SRPX, RBL2, PFDN4, ILK, F2R, ERBB3, and MYB were up-regulated, whereas AKR1C2, FOS, GDF15, NR2F1, ATM, and CTPS were down-regulated after TWIST depletion |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
TWIST1 | down-regulates quantity by repression
transcriptional regulation
|
NF1 |
0.281 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255530 |
|
|
Homo sapiens |
HGC-27 Cell |
pmid |
sentence |
19051271 |
we performed microarray analysis to compare the gene expression profiles in HGC-27 cells, with or without small interfering RNA (siRNA)-mediated depletion of TWIST. Our results showed that NF1, RAP1A, SRPX, RBL2, PFDN4, ILK, F2R, ERBB3, and MYB were up-regulated, whereas AKR1C2, FOS, GDF15, NR2F1, ATM, and CTPS were down-regulated after TWIST depletion |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
TWIST1 | up-regulates quantity by expression
transcriptional regulation
|
CD44 |
0.53 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255512 |
|
|
Homo sapiens |
HEY Cell |
pmid |
sentence |
17487558 |
Immunoblot analysis showed that HEY/si-TWIST cells exhibited decreased expression levels of CD29, CD44 and CD54 compared to those of HEY/si-scrambled cells |
|
Publications: |
1 |
Organism: |
Homo Sapiens |