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Transcriptional changes in response to TGFB in human pancreatic stellate cells with knockdown of PIN1

ABSTRACT: Pancreatic stellate cells can be activated to a myofibroblast phenotype in response to TGFB treatment. The goal of this study was to determine how loss of PIN1 affects stellate cell state at baseline and in response to TGFB treatment.

ORGANISM(S): Homo sapiens

PROVIDER: GSE299852 | GEO | 2025/08/26

REPOSITORIES: GEO

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Transcriptional changes in response to TGFB in human pancreatic stellate cells with inhibition of PIN1

Project description:Pancreatic stellate cells can be activated to a myofibroblast phenotype in response to TGFB treatment. The goal of this study was to determine how inhibition of PIN1 affects stellate cell state at baseline and in response to TGFB treatment.

2025-08-26 | GSE299851 | GEO

Chromatin accessibility changes in response to TGFB in human pancreatic stellate cells with knockdown of PIN1

Project description:Pancreatic stellate cells can be activated to a myofibroblast phenotype in response to TGFB treatment. The goal of this study was to determine how loss of PIN1 affects stellate cell state at baseline and in response to TGFB treatment.

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Transcriptional changes in response to TGFB in human pancreatic stellate cells with inhibition of PIN1

Project description:Transcriptional changes in response to TGFB in human pancreatic stellate cells with inhibition of PIN1

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Transcriptional changes in response to TGFB in human pancreatic stellate cells with knockdown of PIN1

Project description:Transcriptional changes in response to TGFB in human pancreatic stellate cells with knockdown of PIN1

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Chromatin accessibility changes in response to TGFB in human pancreatic stellate cells with knockdown of PIN1

Project description:Chromatin accessibility changes in response to TGFB in human pancreatic stellate cells with knockdown of PIN1

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Expression data from Pin1 inhibitor ATRA and Pin1 knockdown

Project description:ATRA was identified as a Pin1 inhibitor via fluorescence polarization-based high throughput screening. We performed microarray expression profiling to demonstrate the similarity between ATRA and Pin1 KD at the genome-wide level APL NB4 cells in response to ATRRA or inducible Pin1 knockdown for 3 days were collected for RNA extraction and hybridization on Affymetrix microarrays. We sought to validate in genome-wide level whether similarity occurred between ATRA and Pin1 knockdown-treated NB4 cells.

2015-04-12 | E-GEOD-63059 | biostudies-arrayexpress

Amniotic Fluid Reduces Liver Fibrosis By Attenuating Hepatic Stellate Cell Activation

Project description:Chronic activation of hepatic stellate cells leads to irreversible liver fibrosis, and durable treatment options for liver fibrosis remain suboptimal, creating a critical clinical need. Amniotic fluid (AF) reduces inflammation and promotes tissue remodeling and regeneration when applied to cutaneous wounds and in models thereof. However, no prior studies have explored the anti-fibrotic benefits of AF in liver disease. Data from this study indicate that AF can repress liver fibrosis by reducing hepatic stellate cell myofibroblast activation. Thus, these findings lay the foundation for early-phase clinical trials investigating cell-free AF as a therapeutic treatment for liver fibrosis and as a bridging therapy for liver transplantation

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Expression data from Pin1 inhibitor ATRA and Pin1 knockdown

2015-04-12 | GSE63059 | GEO

Pin1 is required for sustained B cell proliferation upon oncogenic activation of Myc

Project description:The c-myc proto-oncogene is activated by translocation in Burkitt's lymphoma and substitutions in codon 58 stabilize the Myc protein or augment its oncogenic potential. In wild-type Myc, phosphorylation of Ser 62 and Thr 58 provide a landing pad for the peptidyl prolyl-isomerase Pin1, which in turn promotes Ser 62 dephosphorylation and Myc degradation. However, the role of Pin1 in Myc-induced lymphomagenesis remains unknown. We show here that genetic ablation of Pin1 reduces lymphomagenesis in EÂµ-myc transgenic mice. In both Pin1-deficient B-cells and MEFs, the proliferative response to Myc was selectively impaired, with no alterations in Myc-induced apoptosis or mitogen-induced cell cycle entry. This proliferative defect wasn't attributable to alterations in either Ser 62 phosphorylation or Myc-regulated transcription, but to the indirect activation of an Arf-p53 dependent cytostatic response. Pin1 silencing in lymphomas retarded disease progression in mice, making Pin1 an attractive therapeutic target in Myc-driven tumors. RNAseq samples of Pin1+/+ control (n=4), Pin1 -/- control (n=2), Pin1+/+ EÂµ-myc pre-tumoral (n=3), and Pin1-/- EÂµ-myc pre-tumoral (n=4) B cells.

2016-06-14 | E-GEOD-77482 | biostudies-arrayexpress

Selective inhibition of Pin1 with a covalent small molecule targeting its catalytic domain

Project description:From a mechanism-based screening we have identified a novel Pin1 suicide inhibitor, KPT-6566, able to selectively inhibit Pin1 and target it for degradation. We have performed a transcriptiomic analysis comparing Pin1 specific RNA interference in MDA-MB 231 cells with KPT-6566 treatment to assess specificity of the KPT-6566 towards Pin1.

2017-08-11 | GSE84909 | GEO

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