| + |
CSNK1A1 |
phosphorylation
|
LGALS3 |
0.302 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-250789 |
Ser12 |
FSLHDALsGSGNPNP |
in vitro |
|
| pmid |
sentence |
| 8253806 |
L-29, a soluble lactose-binding lectin, is phosphorylated on serine 6 and serine 12 in vivo and by casein kinase I. |
|
| Publications: |
1 |
Organism: |
In Vitro |
| + |
CSNK1A1 | up-regulates 
phosphorylation
|
LGALS3 |
0.302 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-124583 |
Ser6 |
sLHDALSG |
Homo sapiens |
Breast Cancer Cell |
| pmid |
sentence |
| 15121858 |
These results indicate that phosphorylation of gal-3 promotes its nuclear export after apoptotic stimuli through enhanced nuclear export. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
ABL1 |
phosphorylation
|
LGALS3 |
0.352 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-166493 |
Tyr107 |
AYPATGPyGAPAGPL |
Homo sapiens |
|
| pmid |
sentence |
| 20600357 |
In this report we have identified novel tyrosine phosphorylation sites in galectin-3 as well as the kinase responsible for its phosphorylation. Our results demonstrate that tyrosines at positions 79, 107 and 118 can be phosphorylated in vitro and in vivo by c-abl kinase. our results demonstrate that cells expressing galectin-3 y107f variant showed reduced migration in wound healing assay ( fig. 5). This result confirms the role of galectin-3 tyrosine phosphorylation in cell motility. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-166497 |
Tyr118 |
AGPLIVPyNLPLPGG |
Homo sapiens |
|
| pmid |
sentence |
| 20600357 |
In this report we have identified novel tyrosine phosphorylation sites in galectin-3 as well as the kinase responsible for its phosphorylation. Our results demonstrate that tyrosines at positions 79, 107 and 118 can be phosphorylated in vitro and in vivo by c-abl kinase. our results demonstrate that cells expressing galectin-3 y107f variant showed reduced migration in wound healing assay ( fig. 5). This result confirms the role of galectin-3 tyrosine phosphorylation in cell motility. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-166501 |
Tyr79 |
GAPAPGVyPGPPSGP |
Homo sapiens |
|
| pmid |
sentence |
| 20600357 |
In this report we have identified novel tyrosine phosphorylation sites in galectin-3 as well as the kinase responsible for its phosphorylation. Our results demonstrate that tyrosines at positions 79, 107 and 118 can be phosphorylated in vitro and in vivo by c-abl kinase. our results demonstrate that cells expressing galectin-3 y107f variant showed reduced migration in wound healing assay ( fig. 5). This result confirms the role of galectin-3 tyrosine phosphorylation in cell motility. |
|
| Publications: |
3 |
Organism: |
Homo Sapiens |
| + |
ABL2 | up-regulates
phosphorylation
|
LGALS3 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-163743 |
Tyr118 |
AGPLIVPyNLPLPGG |
Homo sapiens |
|
| pmid |
sentence |
| 20150913 |
The sh (src homology)3 domains of c-abl/arg bind to a p(80)gppsgp motif of gal3, and tyr79 and tyr118 are the major tyrosine phosphorylation sites. A consequence of this interaction and phosphorylation is the significant impairment of chaperone-mediated autophagy of gal3. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-163747 |
Tyr79 |
GAPAPGVyPGPPSGP |
Homo sapiens |
|
| pmid |
sentence |
| 20150913 |
The sh (src homology)3 domains of c-abl/arg bind to a p(80)gppsgp motif of gal3, and tyr79 and tyr118 are the major tyrosine phosphorylation sites. A consequence of this interaction and phosphorylation is the significant impairment of chaperone-mediated autophagy of gal3. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| + |
GSK3B | up-regulates quantity by expression 
transcriptional regulation
|
LGALS3 |
0.335 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261903 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 21821001 |
Our study also showed that a number of K562 cells survived despite the apoptotic stimuli. Within these surviving cells, galectin-3 was upregulated through newly synthesized protein. Notably, inducible galectin-3, which stabilized the pro-survival Bcl-2 family proteins Mcl-1, Bcl-xL, and Bcl-2, was essential for anti-apoptosis. Unpredictably, GSK-3β was critical for inducible galectin-3 expression as well as for cell survival. As summarized in Fig. 4C, we not only found inducible galectin-3 has an anti-apoptotic effect, but we also identified a GSK-3β-regulated mechanism for apoptotic resistance in K562 cells. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
LGALS3 | up-regulates quantity by stabilization
|
MCL1 |
0.253 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261905 |
|
|
Homo sapiens |
K-562 Cell |
| pmid |
sentence |
| 21821001 |
Our study also showed that a number of K562 cells survived despite the apoptotic stimuli. Within these surviving cells, galectin-3 was upregulated through newly synthesized protein. Notably, inducible galectin-3, which stabilized the pro-survival Bcl-2 family proteins Mcl-1, Bcl-xL, and Bcl-2, was essential for anti-apoptosis. Unpredictably, GSK-3β was critical for inducible galectin-3 expression as well as for cell survival. As summarized in Fig. 4C, we not only found inducible galectin-3 has an anti-apoptotic effect, but we also identified a GSK-3β-regulated mechanism for apoptotic resistance in K562 cells. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
LGALS3 | up-regulates quantity by stabilization
|
BCL2L1 |
0.277 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261906 |
|
|
Homo sapiens |
K-562 Cell |
| pmid |
sentence |
| 21821001 |
Our study also showed that a number of K562 cells survived despite the apoptotic stimuli. Within these surviving cells, galectin-3 was upregulated through newly synthesized protein. Notably, inducible galectin-3, which stabilized the pro-survival Bcl-2 family proteins Mcl-1, Bcl-xL, and Bcl-2, was essential for anti-apoptosis. Unpredictably, GSK-3β was critical for inducible galectin-3 expression as well as for cell survival. As summarized in Fig. 4C, we not only found inducible galectin-3 has an anti-apoptotic effect, but we also identified a GSK-3β-regulated mechanism for apoptotic resistance in K562 cells. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
LGALS3 | up-regulates activity
binding
|
Av/b3 integrin |
0.274 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-277741 |
|
|
Homo sapiens |
Pancreatic Cancer Cell |
| pmid |
sentence |
| 32745890 |
Oncogenic RAS requires a protein scaffold to induce downstream signaling and macropinocytosis, three separate studies have identified upstream and downstream regulators that help drive this process in cancer cells. Anchorage-independent growth of cancer cells is supported by avb3 integrins which can be clustered by the extracellular lectin, galectin-3 to drive mutant RAS-mediated macropinocytosis for nutrient supplementation and growth of anchorage-independent cells. Secreted galectin-3 was found to bind to the N-glycans on surface avb3 integrins, clustering the integrins on the surface of the nonadherent cells for the recruit- ment of mutant KRAS as a signaling platform for inducing macropinocytosis |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
LGALS3 | down-regulates 
|
Apoptosis |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261904 |
|
|
Homo sapiens |
K-562 Cell |
| pmid |
sentence |
| 21821001 |
The aim of this study was to investigate the role of inducible galectin-3 in leukemic cells escape of apoptotic stimuli. Notably, inducible galectin-3, which stabilized the pro-survival Bcl-2 family proteins Mcl-1, Bcl-xL, and Bcl-2, was essential for anti-apoptosis. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
LGALS3 | up-regulates quantity by stabilization
|
BAD |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261907 |
|
|
Homo sapiens |
K-562 Cell |
| pmid |
sentence |
| 21821001 |
Our study also showed that a number of K562 cells survived despite the apoptotic stimuli. Within these surviving cells, galectin-3 was upregulated through newly synthesized protein. Notably, inducible galectin-3, which stabilized the pro-survival Bcl-2 family proteins Mcl-1, Bcl-xL, and Bcl-2, was essential for anti-apoptosis. Unpredictably, GSK-3β was critical for inducible galectin-3 expression as well as for cell survival. As summarized in Fig. 4C, we not only found inducible galectin-3 has an anti-apoptotic effect, but we also identified a GSK-3β-regulated mechanism for apoptotic resistance in K562 cells. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
4.0
LGALS3
- 
- 