+ |
TGFB1 | up-regulates
|
Activated PSC |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-277679 |
|
|
Homo sapiens |
|
pmid |
sentence |
38540204 |
Resident fibroblasts, especially PSC, have the ability to transdifferentiate from a “quiescent” retinoid/lipid storing phenotype in the normal pancreas to an “activated” α-smooth muscle-actin-producing myofibroblastic phenotype through tumor-derived stimuli such as cytokines (interleukin(IL)-1, IL-6, and IL-8 and tumor necrosis factor (TNF)-α), growth factors (platelet-derived growth factor (PDGF) and tumor growth factor (TGF)-β), and reactive oxygen species [33]. Activated PSCs can, in turn, produce autocrine factors such as PDGF, TGF-β, and cytokines, which may contribute to a looping mechanism promoting a desmoplastic reaction |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Tissue: |
Pancreas |
+ |
TGFB2 | up-regulates
|
Activated PSC |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-277680 |
|
|
Homo sapiens |
|
pmid |
sentence |
38540204 |
Resident fibroblasts, especially PSC, have the ability to transdifferentiate from a “quiescent” retinoid/lipid storing phenotype in the normal pancreas to an “activated” α-smooth muscle-actin-producing myofibroblastic phenotype through tumor-derived stimuli such as cytokines (interleukin(IL)-1, IL-6, and IL-8 and tumor necrosis factor (TNF)-α), growth factors (platelet-derived growth factor (PDGF) and tumor growth factor (TGF)-β), and reactive oxygen species [33]. Activated PSCs can, in turn, produce autocrine factors such as PDGF, TGF-β, and cytokines, which may contribute to a looping mechanism promoting a desmoplastic reaction |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Tissue: |
Pancreas |
+ |
A5/b1 integrin | up-regulates
|
Activated PSC |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-277688 |
|
|
Homo sapiens |
|
pmid |
sentence |
32928643 |
CTGF is highly expressed in PDAC tissues, especially in tumor stroma (as shown by immunohistochemistry, CTGF: brown stain). The tumor cell-secreted CTGF promotes pancreatic stellate cell (PSC) proliferation, adhesion, and migration via integrin α5β1, leading to extracellular matrix (ECM) deposition.Pancreatic cancer cells secrete high levels of CTGF that binds to integrin α5β1, promoting PSC proliferation, adhesion, and migration |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
Activated PSC | up-regulates quantity
|
TGFB2 |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-277674 |
|
|
Homo sapiens |
|
pmid |
sentence |
38540204 |
Resident fibroblasts, especially PSC, have the ability to transdifferentiate from a “quiescent” retinoid/lipid storing phenotype in the normal pancreas to an “activated” α-smooth muscle-actin-producing myofibroblastic phenotype through tumor-derived stimuli such as cytokines (interleukin(IL)-1, IL-6, and IL-8 and tumor necrosis factor (TNF)-α), growth factors (platelet-derived growth factor (PDGF) and tumor growth factor (TGF)-β), and reactive oxygen species [33]. Activated PSCs can, in turn, produce autocrine factors such as PDGF, TGF-β, and cytokines, which may contribute to a looping mechanism promoting a desmoplastic reaction |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Tissue: |
Pancreas |
+ |
Activated PSC | up-regulates quantity
|
ACTA2 |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-277677 |
|
|
Homo sapiens |
|
pmid |
sentence |
28232471 |
Upon activa- tion, PSCs express the myofibroblast protein α-smooth mus- cle actin (αSMA, gene name Acta2) and secrete factors that stimulate tumor growth, cell survival, and metastasis. As a result of the selective high expression of αSMA, we refer to these periglandular FAP+ αSMAhigh fibroblasts as myofibroblastic CAFs (myCAFs). |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Tissue: |
Pancreas |
+ |
Activated PSC | up-regulates quantity
|
TGFB1 |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-277673 |
|
|
Homo sapiens |
|
pmid |
sentence |
38540204 |
Resident fibroblasts, especially PSC, have the ability to transdifferentiate from a “quiescent” retinoid/lipid storing phenotype in the normal pancreas to an “activated” α-smooth muscle-actin-producing myofibroblastic phenotype through tumor-derived stimuli such as cytokines (interleukin(IL)-1, IL-6, and IL-8 and tumor necrosis factor (TNF)-α), growth factors (platelet-derived growth factor (PDGF) and tumor growth factor (TGF)-β), and reactive oxygen species [33]. Activated PSCs can, in turn, produce autocrine factors such as PDGF, TGF-β, and cytokines, which may contribute to a looping mechanism promoting a desmoplastic reaction |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Tissue: |
Pancreas |