| + |
GSK3B | down-regulates 
phosphorylation
|
SNAI1 |
0.562 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-129398 |
Ser100 |
DEDSGKGsQPPSPPS |
Homo sapiens |
|
| pmid |
sentence |
| 15448698 |
Snail is a well-known zn-finger transcription factor that promotes emt by repressing e-cadherin expression. It is known that snail is phosphorylated by gsk3beta and degraded by beta-trcp-mediated ubiquitination. A variant of snail (snail-6sa), which abolishes these phosphorylations, is much more stable and resides exclusively in the nucleus to induce emt |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-164613 |
Ser100 |
DEDSGKGsQPPSPPS |
Homo sapiens |
|
| pmid |
sentence |
| 20305697 |
Snail is a well-known zn-finger transcription factor that promotes emt by repressing e-cadherin expression. It is known that snail is phosphorylated by gsk3beta and degraded by beta-trcp-mediated ubiquitination. A variant of snail (snail-6sa), which abolishes these phosphorylations, is much more stable and resides exclusively in the nucleus to induce emt |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-129402 |
Ser104 |
GKGSQPPsPPSPAPS |
Homo sapiens |
|
| pmid |
sentence |
| 15448698 |
Snail is a well-known zn-finger transcription factor that promotes emt by repressing e-cadherin expression. It is known that snail is phosphorylated by gsk3beta and degraded by beta-trcp-mediated ubiquitination. A variant of snail (snail-6sa), which abolishes these phosphorylations, is much more stable and resides exclusively in the nucleus to induce emt |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-164617 |
Ser104 |
GKGSQPPsPPSPAPS |
Homo sapiens |
|
| pmid |
sentence |
| 20305697 |
Snail is a well-known zn-finger transcription factor that promotes emt by repressing e-cadherin expression. It is known that snail is phosphorylated by gsk3beta and degraded by beta-trcp-mediated ubiquitination. A variant of snail (snail-6sa), which abolishes these phosphorylations, is much more stable and resides exclusively in the nucleus to induce emt |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-164621 |
Ser107 |
SQPPSPPsPAPSSFS |
Homo sapiens |
|
| pmid |
sentence |
| 20305697 |
Snail is a well-known zn-finger transcription factor that promotes emt by repressing e-cadherin expression. It is known that snail is phosphorylated by gsk3beta and degraded by beta-trcp-mediated ubiquitination. A variant of snail (snail-6sa), which abolishes these phosphorylations, is much more stable and resides exclusively in the nucleus to induce emt |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-129406 |
Ser107 |
SQPPSPPsPAPSSFS |
Homo sapiens |
|
| pmid |
sentence |
| 15448698 |
Snail is a well-known zn-finger transcription factor that promotes emt by repressing e-cadherin expression. It is known that snail is phosphorylated by gsk3beta and degraded by beta-trcp-mediated ubiquitination. A variant of snail (snail-6sa), which abolishes these phosphorylations, is much more stable and resides exclusively in the nucleus to induce emt |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-164625 |
Ser111 |
SPPSPAPsSFSSTSV |
Homo sapiens |
|
| pmid |
sentence |
| 20305697 |
Snail is a well-known zn-finger transcription factor that promotes emt by repressing e-cadherin expression. It is known that snail is phosphorylated by gsk3beta and degraded by beta-trcp-mediated ubiquitination. A variant of snail (snail-6sa), which abolishes these phosphorylations, is much more stable and resides exclusively in the nucleus to induce emt |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-129410 |
Ser111 |
SPPSPAPsSFSSTSV |
Homo sapiens |
|
| pmid |
sentence |
| 15448698 |
Snail is a well-known zn-finger transcription factor that promotes emt by repressing e-cadherin expression. It is known that snail is phosphorylated by gsk3beta and degraded by beta-trcp-mediated ubiquitination. A variant of snail (snail-6sa), which abolishes these phosphorylations, is much more stable and resides exclusively in the nucleus to induce emt |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-164629 |
Ser115 |
PAPSSFSsTSVSSLE |
Homo sapiens |
|
| pmid |
sentence |
| 20305697 |
Snail is a well-known zn-finger transcription factor that promotes emt by repressing e-cadherin expression. It is known that snail is phosphorylated by gsk3beta and degraded by beta-trcp-mediated ubiquitination. A variant of snail (snail-6sa), which abolishes these phosphorylations, is much more stable and resides exclusively in the nucleus to induce emt |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-129414 |
Ser115 |
PAPSSFSsTSVSSLE |
Homo sapiens |
|
| pmid |
sentence |
| 15448698 |
Snail is a well-known zn-finger transcription factor that promotes emt by repressing e-cadherin expression. It is known that snail is phosphorylated by gsk3beta and degraded by beta-trcp-mediated ubiquitination. A variant of snail (snail-6sa), which abolishes these phosphorylations, is much more stable and resides exclusively in the nucleus to induce emt |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-164633 |
Ser119 |
SFSSTSVsSLEAEAY |
Homo sapiens |
|
| pmid |
sentence |
| 20305697 |
Snail is a well-known zn-finger transcription factor that promotes emt by repressing e-cadherin expression. It is known that snail is phosphorylated by gsk3beta and degraded by beta-trcp-mediated ubiquitination. A variant of snail (snail-6sa), which abolishes these phosphorylations, is much more stable and resides exclusively in the nucleus to induce emt |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-129418 |
Ser119 |
SFSSTSVsSLEAEAY |
Homo sapiens |
|
| pmid |
sentence |
| 15448698 |
Snail is a well-known zn-finger transcription factor that promotes emt by repressing e-cadherin expression. It is known that snail is phosphorylated by gsk3beta and degraded by beta-trcp-mediated ubiquitination. A variant of snail (snail-6sa), which abolishes these phosphorylations, is much more stable and resides exclusively in the nucleus to induce emt |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-129422 |
Ser96 |
TSLSDEDsGKGSQPP |
Homo sapiens |
|
| pmid |
sentence |
| 15448698 |
Snail is a well-known zn-finger transcription factor that promotes emt by repressing e-cadherin expression. It is known that snail is phosphorylated by gsk3beta and degraded by beta-trcp-mediated ubiquitination. A variant of snail (snail-6sa), which abolishes these phosphorylations, is much more stable and resides exclusively in the nucleus to induce emt |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-164637 |
Ser96 |
TSLSDEDsGKGSQPP |
Homo sapiens |
|
| pmid |
sentence |
| 20305697 |
Snail is a well-known zn-finger transcription factor that promotes emt by repressing e-cadherin expression. It is known that snail is phosphorylated by gsk3beta and degraded by beta-trcp-mediated ubiquitination. A variant of snail (snail-6sa), which abolishes these phosphorylations, is much more stable and resides exclusively in the nucleus to induce emt |
|
| Publications: |
14 |
Organism: |
Homo Sapiens |
| + |
ATM | up-regulates activity 
phosphorylation
|
SNAI1 |
0.486 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-279587 |
Ser100 |
DEDSGKGsQPPSPPS |
Homo sapiens |
|
| pmid |
sentence |
| 23891091 |
ATM-mediated Snail Serine 100 phosphorylation regulates cellular radiosensitivity. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
DYRK2 | down-regulates activity
phosphorylation
|
SNAI1 |
0.352 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-279328 |
Ser104 |
GKGSQPPsPPSPAPS |
Homo sapiens |
|
| pmid |
sentence |
| 25603354 |
DYRK2 mediated Snail degradation protects against tumor cell metastasis.|DYRK2 phosphorylation of Snail at Ser104 triggers sequential phosphorylation by GSK3. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
PRKD1 | down-regulates activity
phosphorylation
|
SNAI1 |
0.471 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-168537 |
Ser11 |
SFLVRKPsDPNRKPN |
Homo sapiens |
|
| pmid |
sentence |
| 20940406 |
Pkd1 phosphorylates ser(11) (s11) on transcription factor snail, a master emt regulator and repressor of e-cadherin expression, triggering nuclear export of snail via 14-3-3_ binding. Pkd1 regulates the expression of e-cadherin at the promoter level through direct phosphorylation of the transcriptional repressor snai1. Pkd1-mediated phosphorylation of snai1 occurs in the nucleus and generates a nuclear, inactive dna/snai1 complex that shows decreased interaction with its co-repressor ajuba. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
CSNK2A1 | up-regulates quantity by stabilization
phosphorylation
|
SNAI1 |
0.347 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-161771 |
Ser11 |
SFLVRKPsDPNRKPN |
Homo sapiens |
|
| pmid |
sentence |
| 19923321 |
Serines 11 and 92 participate in the control of snail1 stability and positively regulate snail1 repressive function and its interaction with msin3a corepressor. Furthermore, serines 11 and 92 are required for snail1-mediated emt and cell viability, respectively. Pka and ck2 have been characterized as the main kinases responsible for in vitro snail1 phosphorylation at serine 11 and 92, respectively. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
PAK1 | up-regulates
phosphorylation
|
SNAI1 |
0.408 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-135605 |
Ser246 |
QACARTFsRMSLLHK |
Homo sapiens |
Breast Cancer Cell |
| pmid |
sentence |
| 15833848 |
Pak1 regulates the repressor activity of snail by phosphorylating on ser(246). Pak1 phosphorylation of snail supports snail's accumulation in the nucleus as well as its repressor functions. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
PKN1 | up-regulates
phosphorylation
|
SNAI1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-135609 |
Ser246 |
QACARTFsRMSLLHK |
Homo sapiens |
Breast Cancer Cell |
| pmid |
sentence |
| 15833848 |
Pak1 phosphorylation of snail, a master regulator of epithelial-to-mesenchyme transition, modulates snail's subcellular localization and functionswe found for the first time that pak1 promotes transcription repression activity of snail from e-cadherin, occludin, and aromatase promoters. Pak1 regulates the repressor activity of snail by phosphorylating on ser(246). Pak1 phosphorylation of snail supports snail's accumulation in the nucleus as well as its repressor functions. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
PRKCZ | down-regulates quantity by destabilization
phosphorylation
|
SNAI1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-277437 |
Ser249 |
ARTFSRMsLLHKHQE |
Homo sapiens |
MCF-10A Cell |
| pmid |
sentence |
| 30804505 |
APKC kinases phosphorylate S249 of SNAI1, which leads to protein degradation. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
PRKAA1 | up-regulates
phosphorylation
|
SNAI1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-161783 |
Ser92 |
VAELTSLsDEDSGKG |
Homo sapiens |
|
| pmid |
sentence |
| 19923321 |
Serines 11 and 92 participate in the control of snail1 stability and positively regulate snail1 repressive function and its interaction with msin3a corepressor. Furthermore, serines 11 and 92 are required for snail1-mediated emt and cell viability, respectively. Pka and ck2 have been characterized as the main kinases responsible for in vitro snail1 phosphorylation at serine 11 and 92, respectively. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
PRKAA1 | up-regulates quantity by stabilization
phosphorylation
|
SNAI1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-161779 |
Ser92 |
SFLVRKPsDPNRKPN |
Homo sapiens |
|
| pmid |
sentence |
| 19923321 |
Serines 11 and 92 participate in the control of snail1 stability and positively regulate snail1 repressive function and its interaction with msin3a corepressor. Furthermore, serines 11 and 92 are required for snail1-mediated emt and cell viability, respectively. Pka and ck2 have been characterized as the main kinases responsible for in vitro snail1 phosphorylation at serine 11 and 92, respectively. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
CSNK2A1 | up-regulates
phosphorylation
|
SNAI1 |
0.347 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-161775 |
Ser92 |
VAELTSLsDEDSGKG |
Homo sapiens |
|
| pmid |
sentence |
| 19923321 |
Serines 11 and 92 participate in the control of snail1 stability and positively regulate snail1 repressive function and its interaction with msin3a corepressor. Furthermore, serines 11 and 92 are required for snail1-mediated emt and cell viability, respectively. Pka and ck2 have been characterized as the main kinases responsible for in vitro snail1 phosphorylation at serine 11 and 92, respectively. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
LATS2 | up-regulates
phosphorylation
|
SNAI1 |
0.53 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-176647 |
Thr203 |
QGHVRTHtGEKPFSC |
Homo sapiens |
|
| pmid |
sentence |
| 21952048 |
Lats2 kinase potentiates snail1 activity by promoting nuclear retention upon phosphorylation. during tgf_-induced emt lats2 is activated and snail1 phosphorylated at t203. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
STK39 | up-regulates activity
phosphorylation
|
SNAI1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-279128 |
Thr203 |
QGHVRTHtGEKPFSC |
Homo sapiens |
|
| pmid |
sentence |
| 34335956 |
In this study, we found that STK39 also enhances SNAI1 stability by its phosphorylation at T203.|STK39 interacts with SNAI1 and phosphorylates SNAI1 on T203. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
SFN | down-regulates
relocalization
|
SNAI1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-168540 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 20940406 |
Pkd1 phosphorylates ser(11) (s11) on transcription factor snail, a master emt regulator and repressor of e-cadherin expression, triggering nuclear export of snail via 14-3-3_ binding |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
hsa-miR-338-3p | down-regulates quantity by repression 
post transcriptional regulation
|
SNAI1 |
0.4 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-277975 |
|
|
Homo sapiens |
MHCC97-H Cell |
| pmid |
sentence |
| 29069716 |
MHCC-97H cells treated with the miR-338-3p mimic exhibited decreased Snail1 mRNA and protein expression |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
SNAI1 | down-regulates quantity
transcriptional regulation
|
CDH1 |
0.764 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252260 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 19055748 |
Taken together these results suggest that SNAI1 functional blockade is leading to partial re-expression of E-cadherin (i.e. at the level of transcription), to a decrease in PAI-1 and to a more collective migration, while the parental cells expressing SNAI1 have less E-cadherin, more PAI 1, and migrate individually. We suggest that the present study establishes a relation between SNAI1 function, PAI-1 distribution and EMT status. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
SNAI1 | up-regulates quantity by expression 
transcriptional regulation
|
PLAU |
0.325 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252263 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 19055748 |
We demonstrated by both cDNA microarrays and real-time quantitative RT-PCR that the functional blockade of SNAI1 induces a significant decrease of PAI-1 and uPA transcripts. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
ESRRA | down-regulates quantity by repression
transcriptional regulation
|
SNAI1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253799 |
|
|
Homo sapiens |
Bulb |
| pmid |
sentence |
| 15955695 |
In cancer tissue, the expression levels of EAR-2, COUP-TF1, EARgamma, Snail, and Slug decrease, and aromatase expression is then up-regulated through the binding of ERRalpha to S1 and the binding of CREB1 or related factors to CREaro. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
FBXO22 | down-regulates quantity by destabilization
ubiquitination
|
SNAI1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-273446 |
|
|
Homo sapiens |
Breast Cancer Cell Line |
| pmid |
sentence |
| 29945959 |
FBXO22 elicits its antimetastatic effects by targeting SNAIL, a master regulator of EMT and breast cancer metastasis, for ubiquitin-mediated proteasomal degradation in a glycogen synthase kinase 3β phosphorylation-dependent manner. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
TGFb | up-regulates quantity by expression
transcriptional regulation
|
SNAI1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-265251 |
|
|
Homo sapiens |
HeLa Cell |
| pmid |
sentence |
| 29305973 |
Epithelial-mesenchymal transition (EMT) takes place, namely fibrosis, development and cancer. the process of EMT is integral to a number of physiological and disease states. TGF-β1 is a major effector of this process that activates various key transcription factors such as Snai1. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
SNAI1 | up-regulates
|
Metastasis |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-278098 |
|
|
Homo sapiens |
Hep-G2 Cell |
| pmid |
sentence |
| 27239445 |
We also observed that SNAI1 expression was correlated with distal metastasis, incomplete tumor capsule formation, and histological differentiation in hepatocellular carcinoma (HCC). |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
SNAI1 | form complex 
binding
|
SNAIL/RELA/PARP1 |
0.432 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254526 |
|
|
Homo sapiens |
Fibroblast, Mesenchymal Cell |
| pmid |
sentence |
| 22223884 |
Therefore, we conclude that the endogenous proteins PARP1, p65NF-κB and Snail1 form a ternary complex in the nuclei of cells that are actively expressing fibronectin |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
LATS2 | up-regulates quantity by stabilization
phosphorylation
|
SNAI1 |
0.53 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-272138 |
|
|
in vitro |
|
| pmid |
sentence |
| 24157836 |
FBXL5 is located in the nucleus where it interacts with Snail1 promoting its polyubiquitination and affecting Snail1 protein stability and function by impairing DNA binding. Snail1 is ubiquitinated by the SCFFBXL5 complex. Snail1 downregulation by FBXL5 is prevented by Lats2, a protein kinase that phosphorylates Snail1 precluding its nuclear export but not its polyubiquitination. |
|
| Publications: |
1 |
Organism: |
In Vitro |
| + |
Cullin 1-RBX1-Skp1 | down-regulates quantity by destabilization
ubiquitination, polyubiquitination
|
SNAI1 |
0.269 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-273447 |
|
|
Homo sapiens |
Breast Cancer Cell Line |
| pmid |
sentence |
| 29945959 |
FBXO22 elicits its antimetastatic effects by targeting SNAIL, a master regulator of EMT and breast cancer metastasis, for ubiquitin-mediated proteasomal degradation in a glycogen synthase kinase 3β phosphorylation-dependent manner. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-272137 |
|
|
in vitro |
|
| pmid |
sentence |
| 24157836 |
FBXL5 is located in the nucleus where it interacts with Snail1 promoting its polyubiquitination and affecting Snail1 protein stability and function by impairing DNA binding. Snail1 is ubiquitinated by the SCFFBXL5 complex. Snail1 downregulation by FBXL5 is prevented by Lats2, a protein kinase that phosphorylates Snail1 precluding its nuclear export but not its polyubiquitination. To demonstrate that FBXL5 has a direct activity on Snail1, we carried out polyubiquitination reactions in vitro. For this we purified Snail1 and the SCFFBXL5 complex from Sf9 insect cells infected with different baculoviruses corresponding to Flag-FBXL5, His-Skp1, HA-Cullin1 and Rbx1 (Supplementary Figure S3C). |
|
| Publications: |
2 |
Organism: |
Homo Sapiens, In Vitro |
| + |
SNAI1 | up-regulates
|
Epithelial-mesenchymal_transition |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-265252 |
|
|
Homo sapiens |
HeLa Cell |
| pmid |
sentence |
| 29305973 |
Our findings show that Snai1 mediates repression of PXDN and consolidate a role for this ECM-modifier during EMT. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-278097 |
|
|
Homo sapiens |
Hep-G2 Cell |
| pmid |
sentence |
| 27239445 |
Compelling evidence has demonstrated that SNAI1 plays a key role in the induction of EMT |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252259 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 19055748 |
Taken together these results suggest that SNAI1 functional blockade is leading to partial re-expression of E-cadherin (i.e. at the level of transcription), to a decrease in PAI-1 and to a more collective migration, while the parental cells expressing SNAI1 have less E-cadherin, more PAI 1, and migrate individually. We suggest that the present study establishes a relation between SNAI1 function, PAI-1 distribution and EMT status. |
|
| Publications: |
3 |
Organism: |
Homo Sapiens |
| + |
SNAI1 | up-regulates quantity by expression
transcriptional regulation
|
SERPINE1 |
0.425 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252262 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 19055748 |
We demonstrated by both cDNA microarrays and real-time quantitative RT-PCR that the functional blockade of SNAI1 induces a significant decrease of PAI-1 and uPA transcripts. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
LBX1 | up-regulates quantity by expression
transcriptional regulation
|
SNAI1 |
0.323 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-266053 |
|
|
Homo sapiens |
HEK-293T Cell |
| pmid |
sentence |
| 19651985 |
Compared with the empty vector, LBX1 induced increased promoter activity of threefold to fourfold and fivefold to sixfold for ZEB1 and Snail1, respectively |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
SNAI1 | down-regulates quantity by repression
transcriptional regulation
|
PXDN |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-265249 |
|
|
Homo sapiens |
HeLa Cell |
| pmid |
sentence |
| 29305973 |
TGF-β1 induced Snai1 binding to the PXDN promoter (as assessed by chromatin immunoprecipitation-PCR) and significantly repressed luciferase reporter gene expression, as did Snai1 overexpression. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
SNAI1 | down-regulates quantity by repression
transcriptional regulation
|
CLDN3 |
0.42 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-281176 |
|
|
Homo sapiens |
Breast Cancer Cell |
| pmid |
sentence |
| 23589827 |
In breast cancer cells, SMAD3 and -4 form a complex with SNAIL1 and repress claudin-3 expression, probably through binding to SMAD binding elements that were found adjacent to SNAIL binding E-box sites on the claudin-3 promoter |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
FBXL5 | down-regulates quantity by destabilization
binding
|
SNAI1 |
0.514 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-272135 |
|
|
in vitro |
|
| pmid |
sentence |
| 24157836 |
FBXL5 is located in the nucleus where it interacts with Snail1 promoting its polyubiquitination and affecting Snail1 protein stability and function by impairing DNA binding. Snail1 is ubiquitinated by the SCFFBXL5 complex. Snail1 downregulation by FBXL5 is prevented by Lats2, a protein kinase that phosphorylates Snail1 precluding its nuclear export but not its polyubiquitination. To demonstrate that FBXL5 has a direct activity on Snail1, we carried out polyubiquitination reactions in vitro. For this we purified Snail1 and the SCFFBXL5 complex from Sf9 insect cells infected with different baculoviruses corresponding to Flag-FBXL5, His-Skp1, HA-Cullin1 and Rbx1 (Supplementary Figure S3C). |
|
| Publications: |
1 |
Organism: |
In Vitro |
| + |
SNAI1 | down-regulates quantity by repression
transcriptional regulation
|
HPGD |
0.294 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254237 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 19010907 |
We show an interaction between Snail and HDAC2 and the binding of HDAC2 to the 15-PGDH promoter. These data suggest that class I HDACs, specifically HDAC2, and the transcriptional repressor Snail play a central role in the suppression of 15-PGDH expression. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
NOTCH1 | up-regulates quantity by expression
transcriptional regulation
|
SNAI1 |
0.593 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-281237 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 23973264 |
Notch also upregulates Snail and stabilizes it under hypoxic conditions in cancer cells |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
STUB1 | down-regulates quantity by destabilization
ubiquitination
|
SNAI1 |
0.293 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-278545 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 30927556 |
These results indicate that CHIP can ubiquitylate and degrade Snail in a GSK\u20103\u03b2\u2010independent manner.|These results suggest that CHIP negatively regulates the stability of Snail through inducing its proteasomal degradation. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
SNAI1 | down-regulates quantity by repression
transcriptional regulation
|
CDH1 |
0.764 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255156 |
|
|
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 |
| + |
SNAI1 | up-regulates activity
|
CTBP1 |
0.474 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254103 |
|
|
Homo sapiens |
MDA-MB-468 Cell |
| pmid |
sentence |
| 19277896 |
We propose that CtBP1 is recruited by SNAI1P at the CLDN7 gene promoter indirectly through another yet to be identified protein. Based on our observations, we propose a model for SNAI1P-mediated down regulation of human CLDN7 gene expression by chromatin remodeling |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
Skp1-Pam E3 | down-regulates quantity by destabilization
polyubiquitination
|
SNAI1 |
0.284 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-272188 |
|
|
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 |
| + |
CREB1 | down-regulates quantity by repression
transcriptional regulation
|
SNAI1 |
0.299 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253797 |
|
|
Homo sapiens |
Aorta Thoracica |
| pmid |
sentence |
| 15955695 |
In cancer tissue, the expression levels of EAR-2, COUP-TF1, EARgamma, Snail, and Slug decrease, and aromatase expression is then up-regulated through the binding of ERRalpha to S1 and the binding of CREB1 or related factors to CREaro. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
TCF7 | up-regulates quantity by expression
transcriptional regulation
|
SNAI1 |
0.258 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-281228 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 40025258 |
Specifically, TCF7 knockdown resulted in decreased levels of N-cadherin, Vimentin, Snail, and Fibronectin 1 (FN1), whereas TCF7 overexpression led to an increase in these proteins (Fig. 3C). |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
SNAI1 | down-regulates quantity by repression
transcriptional regulation
|
CLDN7 |
0.413 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254104 |
|
|
Homo sapiens |
MDA-MB-468 Cell |
| pmid |
sentence |
| 19277896 |
We propose that CtBP1 is recruited by SNAI1P at the CLDN7 gene promoter indirectly through another yet to be identified protein. Based on our observations, we propose a model for SNAI1P-mediated down regulation of human CLDN7 gene expression by chromatin remodeling |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
SNAI1 | up-regulates quantity by expression
transcriptional regulation
|
ZEB1 |
0.327 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-281168 |
|
|
Canidae |
95C 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. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-281169 |
|
|
Homo sapiens |
|
| 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: |
2 |
Organism: |
Canidae, Homo Sapiens |
| + |
SNAI1 | down-regulates quantity by repression
transcriptional regulation
|
OCLN |
0.412 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-281178 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 12668723 |
Transfection experiments with various promoter constructs as well as electrophoretic mobility assays revealed that Snail binds directly to the E-boxes of the promoters of claudin/occludin genes, resulting in complete repression of their promoter activity. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
LEF1 | up-regulates quantity by expression
transcriptional regulation
|
SNAI1 |
0.434 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-281225 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 28670499 |
LEF1 is essential in stem cell maintenance and organ development, especially in its role in epithelial-mesenchymal transition (EMT) by activating the transcription of hallmark EMT effectors including N-Cadherin, Vimentin, and Snail. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
hsa-miR-30a-3p | down-regulates quantity by repression
post transcriptional regulation
|
SNAI1 |
0.4 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-278000 |
|
|
Homo sapiens |
OV-2008 Cell |
| pmid |
sentence |
| 26675258 |
The overexpression of miR-30a restored E-cadherin levels, and inhibited the expression of both vimentin and Snail. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
SNAI1 | down-regulates quantity by repression
transcriptional regulation
|
Claudin |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-281177 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 12668723 |
Transfection experiments with various promoter constructs as well as electrophoretic mobility assays revealed that Snail binds directly to the E-boxes of the promoters of claudin/occludin genes, resulting in complete repression of their promoter activity. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
FBXO45 | down-regulates quantity by destabilization
binding
|
SNAI1 |
0.364 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-272181 |
|
|
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 |
| + |
SNAI1 | up-regulates quantity by expression
transcriptional regulation
|
VIM |
0.431 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-281206 |
|
|
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 |
| + |
SNAI1 | down-regulates quantity by repression
transcriptional regulation
|
CLDN4 |
0.35 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-281179 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 23743355 |
The pro-EMT repressor Snail directly interacts with E-boxes within the promoters of occludin and claudins-3, -4, and -7, but not ZO-1, and suppresses their promoter activities thus reducing mRNA and protein content |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
SNAI1 | down-regulates quantity by repression
transcriptional regulation
|
CLDN7 |
0.413 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-281180 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 23743355 |
The pro-EMT repressor Snail directly interacts with E-boxes within the promoters of occludin and claudins-3, -4, and -7, but not ZO-1, and suppresses their promoter activities thus reducing mRNA and protein content |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
SMAD3/SMAD4 | up-regulates quantity by expression
transcriptional regulation
|
SNAI1 |
0.535 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-281167 |
|
|
Homo sapiens |
HEK-293T Cell |
| pmid |
sentence |
| 18832382 |
In the present study we investigated the molecular mechanisms by which HMGA2 induces EMT. We found that HMGA2 regulates expression of many important repressors of E-cadherin. Among these, we analyzed in detail the zinc-finger transcription factor SNAIL1, which plays key roles in tumor progression and EMT. We demonstrate that HMGA2 directly binds to the SNAIL1 promoter and acts as a transcriptional regulator of SNAIL1 expression. Furthermore, we observed that HMGA2 cooperates with the TGF-beta/Smad pathway in regulating SNAIL1 gene expression. The mechanism behind this cooperation involves physical interaction between these factors, leading to an increased binding of Smads to the SNAIL1 promoter |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
MTA1 | up-regulates quantity by expression
transcriptional regulation
|
SNAI1 |
0.5 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254596 |
|
|
Homo sapiens |
OVCAR-3 Cell |
| pmid |
sentence |
| 18719363 |
MTA1 overexpression resulted in downregulation of E-cadherin and MTA3 expression and enhanced expression of the transcriptional repressors SNAIL and SLUG. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
HMGA2 | up-regulates quantity by expression
transcriptional regulation
|
SNAI1 |
0.386 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-281164 |
|
|
Homo sapiens |
HEK-293T Cell |
| pmid |
sentence |
| 18832382 |
In the present study we investigated the molecular mechanisms by which HMGA2 induces EMT. We found that HMGA2 regulates expression of many important repressors of E-cadherin. Among these, we analyzed in detail the zinc-finger transcription factor SNAIL1, which plays key roles in tumor progression and EMT. We demonstrate that HMGA2 directly binds to the SNAIL1 promoter and acts as a transcriptional regulator of SNAIL1 expression. Furthermore, we observed that HMGA2 cooperates with the TGF-beta/Smad pathway in regulating SNAIL1 gene expression. The mechanism behind this cooperation involves physical interaction between these factors, leading to an increased binding of Smads to the SNAIL1 promoter |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-281165 |
|
|
Homo sapiens |
HEK-293T Cell |
| pmid |
sentence |
| 18832382 |
In the present study we investigated the molecular mechanisms by which HMGA2 induces EMT. We found that HMGA2 regulates expression of many important repressors of E-cadherin. Among these, we analyzed in detail the zinc-finger transcription factor SNAIL1, which plays key roles in tumor progression and EMT. We demonstrate that HMGA2 directly binds to the SNAIL1 promoter and acts as a transcriptional regulator of SNAIL1 expression. Furthermore, we observed that HMGA2 cooperates with the TGF-beta/Smad pathway in regulating SNAIL1 gene expression. The mechanism behind this cooperation involves physical interaction between these factors, leading to an increased binding of Smads to the SNAIL1 promoter |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| + |
SMAD2/SMAD4 | up-regulates quantity by expression
transcriptional regulation
|
SNAI1 |
0.518 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-281166 |
|
|
Homo sapiens |
HEK-293T Cell |
| pmid |
sentence |
| 18832382 |
In the present study we investigated the molecular mechanisms by which HMGA2 induces EMT. We found that HMGA2 regulates expression of many important repressors of E-cadherin. Among these, we analyzed in detail the zinc-finger transcription factor SNAIL1, which plays key roles in tumor progression and EMT. We demonstrate that HMGA2 directly binds to the SNAIL1 promoter and acts as a transcriptional regulator of SNAIL1 expression. Furthermore, we observed that HMGA2 cooperates with the TGF-beta/Smad pathway in regulating SNAIL1 gene expression. The mechanism behind this cooperation involves physical interaction between these factors, leading to an increased binding of Smads to the SNAIL1 promoter |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
SNAI1 | up-regulates quantity by expression
transcriptional regulation
|
ZEB2 |
0.315 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-281170 |
|
|
Homo sapiens |
|
| 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 |
| + |
SNAI1 | up-regulates quantity by expression
transcriptional regulation
|
SNAI2 |
0.413 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-281172 |
|
|
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. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-281173 |
|
|
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: |
2 |
Organism: |
Homo Sapiens |
| + |
GSK3B/Axin/APC | down-regulates quantity by destabilization
phosphorylation
|
SNAI1 |
0.4 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-281175 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 17692821 |
Glycogen synthase kinase-3beta (GSK-3beta) regulates the Snail1 level by degrading Snail1 protein. Glycogen synthase kinase-3β (GSK-3β) has recently been demonstrated to regulate the Snail1 level by phosphorylation, β-TrCP-directed ubiquitination, and proteasomal degradation |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
4.0
SNAI1
- 
- 