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We performed gene expression profiles of human bronchoalveolar epithelial cells (HBEC) transduced with GFP labeled murine focal adhesion kinase (PMX-Purom-GFP-mFAK) or GFP control empty vector counterpart (PMX-Purom-GFP-empty)

ABSTRACT: The goal if this project was to determine the cellular pathways affected by FAK protein overexpression downstream of oncogenic KRAS and RHOA in normal lung epithelium. In addition, we aim to characterize the potential downstream modulators of cell growth and migration upon FAK hyperactivation. We identified pathways in DNA damage, cell growth, apoptosis and cytoskeleton remodeling pertaining to tissue differentiation and carcinogenesis signature respectively.

ORGANISM(S): Homo sapiens

PROVIDER: GSE72470 | GEO | 2016/01/01

SECONDARY ACCESSION(S): PRJNA294109

REPOSITORIES: GEO

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We performed gene expression profiles of human bronchoalveolar epithelial cells (HBEC) transduced with GFP labeled murine focal adhesion kinase (PMX-Purom-GFP-mFAK) or GFP control empty vector counterpart (PMX-Purom-GFP-empty)

Project description:The goal if this project was to determine the cellular pathways affected by FAK protein overexpression downstream of oncogenic KRAS and RHOA in normal lung epithelium. In addition, we aim to characterize the potential downstream modulators of cell growth and migration upon FAK hyperactivation. We identified pathways in DNA damage, cell growth, apoptosis and cytoskeleton remodeling pertaining to tissue differentiation and carcinogenesis signature respectively. For this study, two duplicate samples were analyzed in triplicate arrays for a total of 6 data poinst per condition. The groups compared were PMX-Purom-GFP-mFAK against PMX-Purom-GFP-emty.

2016-07-03 | E-GEOD-72470 | biostudies-arrayexpress

Gene expression profiles of human bronchoalveolar epithelial cells (HBEC) transduced with GFP labeled murine focal adhesion kinase (PMX-Purom-GFP-mFAK) or in combination with SUMO ligase Pias1

2016-02-02 | GSE73280 | GEO

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]

Project description:Gene copy number changes, cancer stem cell (CSC) increases, and platinum chemotherapy resistance contribute to poor prognosis in patients with recurrent high grade serous ovarian cancer (HGSOC). CSC phenotypes involving Wnt-b-catenin and aldehyde dehydrogenase activities, platinum resistance, and tumor initiating frequency are here associated with spontaneous genetic gains, including genes encoding KRAS, MYC and FAK, in a new murine model of ovarian cancer (KMF). Noncanonical FAK signaling was sufficient to sustain human and KMF tumorsphere proliferation, CSC survival, and platinum resistance. Increased FAK tyrosine phosphorylation occurred in HGSOC patient tumors surviving neo-adjuvant platinum and paclitaxel chemotherapy and platinum resistant tumorspheres acquired FAK dependence for growth. Importantly, combining a pharmacologic FAK inhibitor with platinum overcame chemoresistance and triggered apoptosis in vitro and in vivo. Knockout, rescue, genomic and transcriptomic analyses collectively identified more than 400 genes regulated along a FAK/b-catenin/Myc axis impacting stemness and DNA repair in HGSOC, with 66 genes gained in a majority of Cancer Genome Atlas samples. Together, these results support combinatorial testing of FAK inhibitors for the treatment of recurrent ovarian cancer.

2019-07-01 | GSE129098 | GEO

Live imaging of GFP-labeled proteins in Drosophila oocytes.

Project description: Not available

| S-EPMC3641710 | biostudies-other

The structures of a naturally empty cowpea mosaic virus particle and its genome-containing counterpart by cryo-electron microscopy.

Project description: Not available

| S-EPMC5428714 | biostudies-literature

In vivo analysis of interactions between GFP-labeled microfilaments and plastid stromules.

Project description: Not available

| S-EPMC356911 | biostudies-literature

Development and characterization of selective FAK inhibitors and PROTACs with in vivo activity

Project description:Focal adhesion kinase (FAK) is an attractive drug target due to its overexpression in cancer. FAK functions as a non-receptor tyrosine kinase and scaffolding protein, coordinating several downstream signaling effectors and cellular processes. While drug discovery efforts have largely focused on targeting FAK kinase activity, FAK inhibitors have failed to show efficacy as single agents in clinical trials. Here, using structure-guided design, we report the development of a selective FAK inhibitor (BSJ-04-175) and degrader (BSJ-04-146) to evaluate the consequences and advantages of abolishing all FAK activity in cancer models. BSJ-04-146 achieves rapid and potent FAK degradation with high proteome-wide specificity in cancer cells and induces remarkably durable degradation in tumor-bearing mice. Compared to kinase inhibition, targeted degradation of FAK exhibits pronounced improved activity on downstream signaling and cancer cell viability and migration. Together, BSJ-04-175 and BSJ-04-146 are valuable chemical tools to dissect the specific consequences of targeting FAK through small molecule inhibition or degradation.

2023-04-26 | PXD039215 | Pride

Development and characterization of selective FAK inhibitors and PROTACs with in vivo activity

2023-04-26 | PXD039254 | Pride

Transcription profiling of mouse cranial neural crest cells of E11.5 wild type and FAK mutants (valle-affy-mouse-480721)

Project description:Cranial neural crest cells (NCC) give rise to the majority of the cartilage, bone, connective tissue, and sensory ganglia in the head, and also participate in the remodeling of the cardiac outflow tract and pharyngeal arch arteries during cardiovascular development. Our preliminary results show that targeted deletion of focal adhesion kinase (FAK) in murine NCC results in cardiovascular and craniofacial alterations, resembling human congenital heart diseases The objective of this project is to elucidate the underlying mechanisms by which FAK mediates NCC function during development. Compare gene expression in cranial neural crest cells of E11.5 wild type and FAK mutants. FAK is a tyrosine kinase that transduces integrin and growth factor signaling pathways. Abnormal growth factor signaling leads to cardiovascular malformations caused by deficient cardiac NCC function. However, a direct role for FAK in NCC morphogenesis has not been demonstrated. We will test the hypothesis that FAK is a downstream target of essential growth factor signaling in cranial neural crest cells during development. 1) Generate E11.5 mouse embryos that are either control (FAK+/flox) or NCC specific FAK knockout (Wnt1Cre;FAKflox/flox). 2) Determine genotype by PCR. 3) Dissect head and torax from the different genotypes. 4) Obtain NCC from dissected tissue by magnetic cell sorting using p75 antibody. 5) Prepare total RNA from speciments. We will pool the NCC from 3 different embryos of the same genotype, and send total RNA to TGEN for probe preparation, hybridization and array result analysis.

2008-06-11 | E-GEOD-11149 | biostudies-arrayexpress

Proteomic analysis of IL33-proximal proteins in squamous cell carcinoma cells

Project description:Focal adhesion kinase (FAK) is required for the expression of pro-inflammatory genes that inhibit anti-tumour immunity. Here, we show a novel and crucial role for the dual-function cytokine IL33 in FAK-dependent immune evasion. Specifically, nuclear FAK is required for the expression of IL33, the chemokine Ccl5 and the soluble form of the IL33 receptor, sST2, which are required for evasion of CD8+ T-cell-mediated anti-tumour immunity. Mechanistically, nuclear IL33 associates with FAK and a network of chromatin modifiers and transcriptional regulators, including Taf9, WDR82 and BRD4, while sST2 likely negates effects of IL33 secreted into the tumour microenvironment by infiltrating host immune cells. Finally, protein interaction network analysis implies that nuclear FAK–IL33 complexes impact on transcription factors that regulate NFkB and chemokines like Ccl5 downstream. Our data therefore provide new mechanistic insight into how FAK controls the tumour immune environment via a FAK–IL33/sST2 pathway and demonstrate a novel role for nuclear IL33 downstream of FAK as a component of transcription regulatory complexes that critically modulate anti-tumour immunity.

2017-12-06 | PXD007698 | Pride

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