| + |
MTA1 | up-regulates quantity by expression 
transcriptional regulation
|
CXCL1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254598 |
|
|
Homo sapiens |
OVCAR-3 Cell |
| pmid |
sentence |
| 18719363 |
Screening for the expression of angiogenic cytokines expressed by ovarian cancer cells revealed MTA1-mediated upregulation of the oncogenic and angiogenic cytokine GRO (growth-regulated oncogene, CXCL1). |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
CXCL1 | up-regulates activity 
binding
|
CXCR2 |
0.788 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-277717 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 38309677 |
CXCL1 produces cellular chemotactic activity by binding to the CXC chemokine receptor 2 (CXCR2). In PC, this chemokine has been associated with a variety of carcinogenic mechanisms, including oncogene-induced senescence (OIS), angiogenesis, cancer metastasis, and immunosuppressive microenvironments |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
CEBPD | up-regulates quantity by expression
transcriptional regulation
|
CXCL1 |
0.271 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254060 |
|
|
Mus musculus |
Macrophage |
| pmid |
sentence |
| 23028973 |
CEBPD activated in macrophages played a functional role in promoting the tube formation of endothelial cells and the migration and proliferation of synoviocytes. In vivo DNA binding assays and reporter assays showed that CEBPD up-regulated CCL20, CXCL1, IL23A and TNFAIP6 transcripts through direct binding to their promoter regions. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
hsa-miR-141-5p | down-regulates quantity by repression 
post transcriptional regulation
|
CXCL1 |
0.4 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-278007 |
|
|
Homo sapiens |
A-549 Cell |
| pmid |
sentence |
| 25349304 |
MiR141 regulated expression of CXCL1 in lung cancer cells, whereas the luciferase test confirmed that CXCL1 is a target of miR141.| hese results of tumor models above demonstrated that miR141 has a potency to inhibit tumor progression through restraining the recruitment of Tregs by inhibiting the production of CXCL1. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
CXCL1 | up-regulates quantity by expression
transcriptional regulation
|
GLI3 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-148460 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 16885213 |
The data suggest that smo is in fact the source of two signals relevant to the activation of gli: one involving g(i) and the other involving events at smo's c-tail independent of g(i). |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
CXCL1 | up-regulates quantity by expression
transcriptional regulation
|
GLI2 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-148457 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 16885213 |
The data suggest that smo is in fact the source of two signals relevant to the activation of gli: one involving g(i) and the other involving events at smo's c-tail independent of g(i). |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
Cyclopamine | down-regulates
chemical inhibition
|
CXCL1 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-148469 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 16885213 |
Cyclopamine and other inhibitors of hh signaling were found to inhibit smo coupling to gi in a manner consistent with inverse agonism. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
SMO | up-regulates
binding
|
CXCL1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-148484 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 16885213 |
We found that smo, by virtue of what appears to be constitutive activity, activates all members of the g(i) family but does not activate members of the g(s), g(q), and g(12) families. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
CXCL1 | down-regulates
binding
|
PRKACA |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-152594 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 17251915 |
As pka suppresses the activity of gli, smo might use the stimulation of pi3k by galfai and gbetagamma subu- nits to block pka in cells that have high levels of camp. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
CXCL1 | up-regulates
|
GLI1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-148454 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 16885213 |
The data suggest that smo is in fact the source of two signals relevant to the activation of gli: one involving g(i) and the other involving events at smo's c-tail independent of g(i). |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NfKb-p65/p50 | up-regulates quantity by expression
transcriptional regulation
|
CXCL1 |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-282636 |
|
|
Homo sapiens |
PANC-1 Cell |
| pmid |
sentence |
| 37541772 |
Our results showed that CRIP1 was frequently upregulated in PDAC tissues with low immune activation. Elevated CRIP1 expression induced high levels of myeloid-derived suppressor cell (MDSC) infiltration and fostered an immunosuppressive tumour microenvironment. Mechanistically, we primarily showed that CRIP1 bound to nuclear factor kappa-B (NF-κB)/p65 and facilitated its nuclear translocation in an importin-dependent manner, leading to the transcriptional activation of CXCL1/5. PDAC-derived CXCL1/5 facilitated the chemotactic migration of MDSCs to drive immunosuppression. SX-682, an inhibitor of CXCR1/2, blocked tumour MDSC recruitment and enhanced T-cell activation. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
ZC3H12A | down-regulates quantity by destabilization
post transcriptional regulation
|
CXCL1 |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-282638 |
|
|
Homo sapiens |
PANC-1 Cell |
| pmid |
sentence |
| 37814340 |
Pancreatitis is known to be an important risk factor for pancreatic ductal adenocarcinoma (PDAC). However, the exact molecular mechanisms of how inflammation promotes PDAC are still not fully understood. Regnase-1, an endoribonuclease, regulates immune responses by degrading mRNAs of inflammation-related genes. Herein, we investigated the role of Regnase-1 in PDAC.Mechanistically, Regnase-1 directly negatively regulated a variety of chemokines/cytokines important for MDSC recruitment and activation, including CXCL1, CXCL2, CSF2, and TGFβ, in pancreatic cancer cells. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
FZD3 | up-regulates
binding
|
CXCL1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-122886 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 14977528 |
In the non-canonical wnt pathway, frizzled uses galfaq or galfai and gbetagamma dimers to activate phospholipase c (plc), resulting in protein kinase c (pkc) activation and calcium mobilization that regulates the transcription factor nfat, and frizzled also signals through the small gtpases rho and rac to c-jun n-terminal kinase (jnk), which activates the ap1 transcription factor gpcrs signal through four relatively small families of galfa proteins (galfas, galfai/o, galfaq, and galfa12/13), and if fzd receptors are classic gpcrs, they should signal through one of these four galfa families. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-152597 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 17251915 |
In the non-canonical wnt pathway, frizzled uses galfaq or galfai and gbetagamma dimers to activate phospholipase c (plc), resulting in protein kinase c (pkc) activation and calcium mobilization that regulates the transcription factor nfat, and frizzled also signals through the small gtpases rho and rac to c-jun n-terminal kinase (jnk), which activates the ap1 transcription factor gpcrs signal through four relatively small families of galfa proteins (galfas, galfai/o, galfaq, and galfa12/13), and if fzd receptors are classic gpcrs, they should signal through one of these four galfa families. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| + |
CXCL1 | up-regulates
|
Neutrophil_activation |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-277721 |
|
|
Homo sapiens |
Neutrophil |
| pmid |
sentence |
| 35022267 |
Chemotherapy-induced infiltration of neutrophils promotes pancreatic cancer metastasis via Gas6/AXL signalling axis. neutrophils are recruited to the metastatic liver via CXCL1 and 2 secretion by metastatic tumour cells. These neutrophils express growth arrest specific 6 (Gas6) which leads to AXL receptor activation on tumour cells enabling their regrowth.Taken together, these results show that the neutrophil attracting cytokines Cxcl1 and 2 are highly expressed in metastatic livers in response to gemcitabine withdrawal and this favours CXCR2-dependent recruitment of neutrophils at the hepatic metastatic site. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
CXCL1 | up-regulates
binding
|
PLCE1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-152591 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 17251915 |
In the non-canonical wnt pathway, frizzled uses galfaq or galfai and gbetagamma dimers to activate phospholipase c (plc), resulting in protein kinase c (pkc) activation and calcium mobilization that regulates the transcription factor nfat, and frizzled also signals through the small gtpases rho and rac to c-jun n-terminal kinase (jnk), which activates the ap1 transcription factor. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
4.0
CXCL1
- 
- 