| + |
IKBKB | down-regulates activity 
phosphorylation
|
TWIST1 |
0.326 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-278405 |
Ser123 |
RERQRTQsLNEAFAA |
Homo sapiens |
|
| pmid |
sentence |
| 23375009 |
Hence, our current study supports the pivotal role of beta-TRCP in IKKbeta mediated Twist degradation.|More importantly, IKKbeta dependent phosphorylation of Twist at T125 and S127 governs its nuclear localization. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-278404 |
Thr121 |
NVRERQRtQSLNEAF |
Homo sapiens |
|
| pmid |
sentence |
| 23375009 |
Hence, our current study supports the pivotal role of beta-TRCP in IKKbeta mediated Twist degradation.|More importantly, IKK\u03b2-dependent phosphorylation of Twist at T125 and S127 governs its nuclear localization. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| + |
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 |
| + |
AKT1 | up-regulates
phosphorylation
|
TWIST1 |
0.432 |
| 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 |
| + |
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 |
| + |
AKT2 | up-regulates activity
phosphorylation
|
TWIST1 |
0.394 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-279137 |
Ser42 |
GGRKRRSsRRSAGGG |
Homo sapiens |
|
| pmid |
sentence |
| 26759241 |
AKT2 phosphorylates Twist1 at S42 to enhance Twist1 mediated E-cadherin suppression. |
|
| 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 |
| + |
MAPK8 | up-regulates
phosphorylation
|
TWIST1 |
0.305 |
| 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 |
| + |
MAPK3 | up-regulates
phosphorylation
|
TWIST1 |
0.325 |
| 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 |
| + |
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 |
| + |
MAPK14 | up-regulates
phosphorylation
|
TWIST1 |
0.267 |
| 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 |
| + |
MAPK1 | up-regulates
phosphorylation
|
TWIST1 |
0.301 |
| 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 |
| + |
TWIST1 | up-regulates quantity by expression 
transcriptional regulation
|
CD44 |
0.561 |
| 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 |
| + |
POU2F1 | up-regulates quantity by expression
transcriptional regulation
|
TWIST1 |
0.256 |
| 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 |
| + |
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
|
ITGB1 |
0.289 |
| 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 |
| + |
RUNX2 | up-regulates quantity by expression
transcriptional regulation
|
TWIST1 |
0.44 |
| 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 |
| + |
EZH2 | down-regulates quantity by repression
transcriptional regulation
|
TWIST1 |
0.327 |
| 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 |
| + |
TWIST1 | down-regulates quantity by repression
transcriptional regulation
|
CDH1 |
0.476 |
| 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 |
| + |
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 |
| + |
SUZ12 | down-regulates quantity by repression
transcriptional regulation
|
TWIST1 |
0.276 |
| 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 |
| + |
HMGA2 | up-regulates quantity by expression
transcriptional regulation
|
TWIST1 |
0.4 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-281171 |
|
|
Homo sapiens |
HEK-293T Cell |
| pmid |
sentence |
| 18832382 |
We then analyzed the effect of Snail1 depletion on expression of the other four E-cadherin repressors, whose levels become increased by HMGA2 overexpression, Snail2, ZEB1, ZEB2, and Twist in the same panel of cells (Fig. 7, A–C). Depletion of the induced Snail1 levels by the shRNA led to a concomitant and significant decrease in Snail2, ZEB1, and ZEB2 mRNA levels. In the case of ZEB1 and ZEB2, their expression was decreased almost down to the levels of the parental epithelial cells (NMuMG-m). In contrast, Twist levels remained unaltered by the knock-down of endogenous Snail1 (Fig. 7C). These results demonstrate that Snail1 regulates specifically the expression of Snail2, ZEB1, and ZEB2 but not that of Twist. The data suggest that HMGA2 causes EMT by inducing at least two primary transcriptional mediators of this process, Snail1 and Twist. |
|
| 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
|
GDF15 |
0.275 |
| 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 |
| + |
TWIST1 | up-regulates quantity by expression
transcriptional regulation
|
VIM |
0.484 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-281203 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 34638469 |
These signalling cascades are also implicated in the induction of EMT via the transcriptional control of EMT-associated transcription factors, such as SNAI1, TWIST, ZEB1, SLUG and TCF3 leading to vimentin expression, as described above (Figure 2). |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
TWIST1 | up-regulates quantity by expression
transcriptional regulation
|
ICAM1 |
0.263 |
| 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 |
| + |
FBXO45 | down-regulates quantity by destabilization
binding
|
TWIST1 |
0.259 |
| 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 | down-regulates quantity by repression
transcriptional regulation
|
MYB |
0.245 |
| 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 |
| + |
TWIST1 | up-regulates quantity by expression
transcriptional regulation
|
MMP2 |
0.371 |
| 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 | up-regulates quantity by expression
transcriptional regulation
|
ATM |
0.287 |
| 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
|
ILK |
0.28 |
| 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 |
| + |
Skp1-Pam E3 | down-regulates quantity by destabilization
polyubiquitination
|
TWIST1 |
0.249 |
| 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 |
| + |
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 |
| + |
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 |
| + |
LIMK2 | up-regulates quantity
phosphorylation
|
TWIST1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-278952 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 30716360 |
LIMK2 directly phosphorylated TWIST1, indicating that LIMK2 also regulates TWIST1 post-translationally (XREF_FIG).|LIMK2 positively regulates TWIST1 protein levels. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
TWIST1 | up-regulates quantity by expression
transcriptional regulation
|
NR2F1 |
0.249 |
| 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 destabilization
post transcriptional regulation
|
hsa-mir-200b-3p |
0.4 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-281210 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 20473948 |
The miR-200 family (miR-200a, -200b, -200c, -141 and -429) and miR-205 are frequently silenced in advanced cancer and have been implicated in epithelial to mesenchymal transition (EMT) and tumor invasion by targeting the transcriptional repressors of E-cadherin, ZEB1 and ZEB2. ZEB1 is also known to repress miR-200c-141 transcription in a negative feedback loop, but otherwise little is known about the transcriptional regulation of the miR-200 family and miR-205. TWIST1 associates directly with the miR-200 and miR-205 promoters, and may act as a repressor of miR-200 and miR-205 expression. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
TWIST1 | up-regulates quantity by expression
transcriptional regulation
|
FN1 |
0.405 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-281220 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 30591455 |
Basic helix-loop-helix transcription factor Twist1 has been described as a master regulator of EMT, repressing the expression of epithelial phenotype markers responsible for cell–cell interaction such as E-cadherin, and at the same time inducing the expression of mesenchymal genes such as Vimentin and Fibronectin, which are involved in cancer cell mobility and invasion |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
TWIST1 | up-regulates quantity by expression
transcriptional regulation
|
CDH2 |
0.43 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-281218 |
|
|
Homo sapiens |
PC-3 Cell |
| pmid |
sentence |
| 16585154 |
Depletion of Twist1 mRNA by small interfering RNA resulted in decreased expression of both Twist1 and N-cadherin and the inhibition of cell migration. The effect of Twist1 on induction of N-cadherin mRNA required an E-box cis-element located within the first intron (+2,627) of the N-cadherin gene. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
HDAC2 | down-regulates quantity by repression
transcriptional regulation
|
TWIST1 |
0.373 |
| 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
|
FN1 |
0.405 |
| 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 |
| + |
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 | 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 | up-regulates quantity by expression
transcriptional regulation
|
SNAI2 |
0.469 |
| 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 | down-regulates quantity by repression
transcriptional regulation
|
RUNX2 |
0.44 |
| 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 | down-regulates quantity by repression
transcriptional regulation
|
NF1 |
0.275 |
| 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 |
| + |
ZRANB1 | down-regulates activity
deubiquitination
|
TWIST1 |
0.328 |
| 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 |
| + |
HIF1A | up-regulates quantity by expression
transcriptional regulation
|
TWIST1 |
0.321 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-281239 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 18635960 |
Hypoxia Promotes Cancer Metastasis throughthe Induction of EMT. Regulation of TWIST Expression by HIF-1 and its Critical Rolein Hypoxia Mediated EMT. Repressionof endogenous HIF-1αby siRNA in cells under hypoxia revertedtheTWISTlevels to pre-hypoxic status, demonstrating that HIF-1αis the major regulator ofTWISTexpression. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
TWIST1 | down-regulates quantity by destabilization
post transcriptional regulation
|
hsa-miR-200c-3p |
0.4 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-281211 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 20473948 |
The miR-200 family (miR-200a, -200b, -200c, -141 and -429) and miR-205 are frequently silenced in advanced cancer and have been implicated in epithelial to mesenchymal transition (EMT) and tumor invasion by targeting the transcriptional repressors of E-cadherin, ZEB1 and ZEB2. ZEB1 is also known to repress miR-200c-141 transcription in a negative feedback loop, but otherwise little is known about the transcriptional regulation of the miR-200 family and miR-205. TWIST1 associates directly with the miR-200 and miR-205 promoters, and may act as a repressor of miR-200 and miR-205 expression. |
|
| 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 destabilization
post transcriptional regulation
|
mir-205 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-281208 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 20473948 |
The miR-200 family (miR-200a, -200b, -200c, -141 and -429) and miR-205 are frequently silenced in advanced cancer and have been implicated in epithelial to mesenchymal transition (EMT) and tumor invasion by targeting the transcriptional repressors of E-cadherin, ZEB1 and ZEB2. ZEB1 is also known to repress miR-200c-141 transcription in a negative feedback loop, but otherwise little is known about the transcriptional regulation of the miR-200 family and miR-205. TWIST1 associates directly with the miR-200 and miR-205 promoters, and may act as a repressor of miR-200 and miR-205 expression. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
TWIST1 | down-regulates quantity by destabilization
post transcriptional regulation
|
hsa-miR-200a-3p |
0.4 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-281209 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 20473948 |
The miR-200 family (miR-200a, -200b, -200c, -141 and -429) and miR-205 are frequently silenced in advanced cancer and have been implicated in epithelial to mesenchymal transition (EMT) and tumor invasion by targeting the transcriptional repressors of E-cadherin, ZEB1 and ZEB2. ZEB1 is also known to repress miR-200c-141 transcription in a negative feedback loop, but otherwise little is known about the transcriptional regulation of the miR-200 family and miR-205. TWIST1 associates directly with the miR-200 and miR-205 promoters, and may act as a repressor of miR-200 and miR-205 expression. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
TWIST1 | up-regulates quantity by expression
transcriptional regulation
|
FAP |
0.241 |
| 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 |
| + |
TWIST1 | up-regulates quantity by expression
transcriptional regulation
|
HGF |
0.322 |
| 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 | 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
|
FOS |
0.47 |
| 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
|
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 |
4.0
TWIST1
- 
- 