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FAK activity alters the transcriptional landscape during SMC phenotypic switching

ABSTRACT: Purpose: The goals of this study are to compare the effect of FAK activity on gene expression of NGS-derived RNA-sequencing during vascular remodeling.

ORGANISM(S): Mus musculus

PROVIDER: GSE183143 | GEO | 2021/09/02

REPOSITORIES: GEO

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FAK activity alters the transcriptional landscape during SMC phenotypic switching

Project description:FAK activity alters the transcriptional landscape during SMC phenotypic switching

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Next generation sequencing comparing effects of FFSS, FAK inhibitor and FAK gene deletion.

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FAK is required for suppressing aberrant nuclear mechanotransduction and DNA methylation to prevent vascular injury

Project description:Mechanical forces generated through adhesive interaction of endothelial cells (EC) influence nuclear envelope and thereby gene transcription. Alteration in EC mechanical forces may trigger aberrant gene transcription leading to lethal vascular diseases including acute lung injury (ALI). The intrinsic pathways that instruct EC nuclear-mechanotransduction and thereby maintains vascular homeostasis remain elusive. We have identified focal adhesion kinase (FAK)-mediated mechanotransduction at the nuclear envelope in instructing transcription of EC-barrier protective genes. We show that loss of EC-FAK increases intracellular tension, which in turn activates nuclear envelop protein emerin, and DNA methyltransferase 3a (DNMT3a). Methylation of transcription factor KLF2 promoter by DNMT3a impaired KLF2 synthesis and transcription of the crucial barrier-maintaining gene, S1PR1. Restoring KLF2 or S1PR1 expression or impairing emerin or DNMT3a activity rescued vascular homeostasis in lungs with FAK-deficient or WT-damaged endothelium. Thus, FAK protects against tension-induced aberrant DNA methylation in EC and is a promising target to prevent ALI.

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Next generation sequencing comparing effects of FFSS, FAK inhibitor and FAK gene deletion. [FFSS]

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ERG activity is regulated by endothelial FAK coupling with TRIM25/USP9x in vascular patterning

Project description:Precise vascular patterning is critical for normal growth and development. The ERG transcription factor drives Delta like ligand 4 (DLL4)/Notch signalling and is thought to act as pivotal regulators of endothelial cell (EC) dynamics and developmental angiogenesis. However, molecular regulation of ERG activity remains obscure. Using a series of EC specific Focal Adhesion Kinase (FAK)-knockout (KO) and point-mutant FAK-knockin mice, we show that loss of ECFAK, its kinase activity or phosphorylation at FAK-Y397, but not FAK-Y861, reduces ERG and DLL4 expression levels together with concomitant aberrations in vascular patterning. Rapid Immunoprecipitation Mass Spectrometry of Endogenous Proteins identified that endothelial nuclear-FAK interacts with the de-ubiquitinase USP9x and the ubiquitin ligase TRIM25 enzymes. Further in silico analysis corroborates that ERG interacts with USP9x and TRIM25. Moreover, ERG levels are reduced in FAKKO ECs via a ubiquitin-mediated post-translational modification programme involving USP9x and TRIM25. Re-expression of ERG in vivo and in vitro rescues the aberrant vessel sprouting defects observed in the absence of ECFAK. Our findings identify ECFAK as a regulator of retinal vascular patterning by controlling ERG protein degradation via TRIM25/USP9x.

2022-07-05 | PXD033447 | Pride

Role of FAK, dominant-negative FAK, FAK-CD and FAKsiRNA in MCF-7 human breast cancer cell tumorigenesis

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FAK activity sustains intrinsic and acquired ovarian cancer resistance to platinum chemotherapy [KMF parental, KMF clone KT13 (FAK-/-), KT13 + GFP-FAK, KT13 + GFP-FAK R454, and KT13 + deltaGSK beta-catenin]

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pCMV-FRNK/pCMV-FAK vs pCMV-FAK in CTL

Project description:CMV-driven inhibition of FAK in soleus muscle was compared vs contralateral muscle

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siRNA profiling if human MCF-7 cell line to investigate the role of FAK, dominant-negative FAK, FAK-CD and FAKsiRNA in MCF-7 human breast cancer cell tumorigenesis

2009-08-22 | E-GEOD-11581 | biostudies-arrayexpress

Gene profile of breast cancer tumors with low and high FAK expression

Project description:The gene expression profiles were identified in breast cancer tumors with different level of FAK three tumors with low FAK expression identified by IHC and 3 tumors with high FAK expression. 2 triple-negative with low and one triple negative with high FAK expression was among these 6 samples

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