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TRIM67 drives tumorigenesis in oligodendrogliomas through Rho GTPase-dependent membrane blebbing

ABSTRACT: TRIM67 drives tumorigenesis in oligodendrogliomas through Rho GTPase-dependent membrane blebbing

PROVIDER: PRJNA765042 | ENA |

REPOSITORIES: ENA

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TRIM67 drives tumorigenesis in oligodendrogliomas through Rho GTPase-dependent membrane blebbing

Project description:The aim of this study is to characterize the mechanistic role of TRIM67 in glioma biogenesis. Towards this goal, here we utilized engineered human neural stem cells and patient-derived tumor sphere lines with or without IDH mutations and 1p/19q co-deletions to study the function of TRIM67 in gliomas. We found that upregulated TRIM67 induces membrane blebbing through Rho GTPase-mediated signaling, resulting in more advanced cell motility and tumor expansion.

2022-09-21 | GSE184567 | GEO

Transcriptional regulation by the novel Rho GTPase RhoBTB2.

2008-08-20 | GSE8837 | GEO

Quantitative GTPase affinity purification identifies Rho family protein interaction partners

Project description:Although Rho GTPases are essential molecular switches involved in many cellular processes, an unbiased experimental comparison of their interaction partners was not yet performed. Here, we develop quantitative GTPase affinity purification (qGAP) to systematically identify interaction partners of six Rho GTPases (Cdc42, Rac1, RhoA, RhoB, RhoC, RhoD) depending on their nucleotide loading state. We use Stable isotope labeling by Amino acids in cell culture (SILAC) and label free quantification (LFQ). Our interaction network contains many new proteins, reveals highly promiscuous binding of several effectors and mirrors evolutionary relationships of Rho GTPases.

2016-12-23 | PXD004190 | Pride

Extracellular Superoxide Dismutase Regulates the Expression of GTPase Guanine Nucleotide Exchange Factors (GEFs), GTPase-activating proteins (GAPs), and Rho Guanine nucleotide disassociation inhibitors (GDI)

Project description:Extracellular superoxide dismutase (SOD3), which dismutases hydrogen peroxide to superoxide anion at cell membranes, mimics RAS oncogene action inducing primary cell immortalization at sustained low-level expression while high expression activates cancer barrier signaling through p53-p21 growth arrest pathway. We have previously demonstrated that the growth regulation of SOD3 occurs at the level of RAS and is mediated through non-transcriptional and transcriptional routes. Therefore, in the current work we assayed the growth suppressive mechanisms of SOD3 by characterizing the main signal transduction routes from the cell membrane into the nucleus. Based on our data robust over-expression of SOD3 in anaplastic thyroid cancer 8505c cells increased EGFR, RYK, ALK, FLT3, and EPHA10 tyrosine kinase receptor phosphorylation with consequent downstream SRC, FYN, YES, HCK, and LYN kinase activation. However, RAS pull-down experiment suggested lack of mitogen pathway stimulation that was confirmed by MEK1/2 and ERK1/2 Western blot. Interestingly, mRNA expression analysis indicated that SOD3 regulated in a dose dependent manner the expression of selected guanine nucleotide exchange factors (Rho GEF16, Ral GEF RGL1), GTPase activating proteins (ArfGAP ADAP2, Ras GAP RASAL1, RGS4), and Rho guanine nucleotide disassociation inhibitors (Rho GDI 2) therefore controlling the signal transduction through RAS GTPases to downstream signal transduction pathways. Our current data suggests a SOD3-induced activation of growth signal transduction is controlled in a dose dependent manner through GEF, GAP, and GDI.

2014-12-31 | GSE56546 | GEO

Ota2015 - Positive regulation of Rho GTPase activity by RhoGDIs as a result of their direct interaction with GAPs (GDI integrated)

Project description:This is a ordinary differential equation mathematical model describing the Rho GTPase cycle in which Rho GDP-dissociation inhibitors (RhoGDIs) inhibit the regulatory activities of guanine nucleotide exchange factors (GEFs) and GTPase-activating proteins (GAPs) by interacting with them directly as well as by sequestering the Rho GTPases. The model was constructed with the intent of analyzing the role of RhoGDIs in Rho GTPase signaling.

2024-09-02 | BIOMD0000000899 | BioModels

An RNAi Screen for Skin Morphogenesis Unravels The Complexities of Rho GTPase Networks

Project description:During embryogenesis, antagonism and synergy between developmental signaling pathways dictate cell fate decisions. How these circuits orchestrate the complex cellular remodeling needed for tissue morphogenesis remains poorly understood. As effectors of cytoskeletal dynamics, Rho GTPases and their regulators are likely to be involved. However, their daunting complexity has hindered progress in dissecting their functions. Here we overcome this hurdle by developing an unbiased, high throughput RNAi-mediated screening approach to identify physiological regulators of morphogenesis. Exploiting in utero lentiviral delivery methods to transduce embryonic mouse skin progenitors, we screened for Rho GTPases and GTPase regulators that differentially function in epidermal versus hair follicle development. Our screen unveiled hitherto unrecognized roles for specific family members in cytoskeletal remodeling events that impact these diverse morphogenetic processes, including epidermal differentiation, follicle downgrowth and planar cell polarity. Our findings underscore the power of our screening strategy for unravel the physiological significance of complex gene families.

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Transcription profiling of primary lung cells to identify targets of the novel Rho GTPase RhoBTB2.

Project description:RhoBTB2 is a novel Rho GTPase that undergoes loss, underexpression and mutation in breast and lung cancer. We have shown that we can mimic loss of RhoBTB2 through siRNA treatment of primary cells. We propose to perform comparative microarray analysis of primary lung cells to establish the identification of the gene targets of RhoBTb2 regulation. Experiment Overall Design: Primary lung cells (NHBE) transfected with siRNA oligonucleotides against cyclophilin or Lamin A/C (controls) were compared to cells transfected with siRNA oligonucleotides against RhoBTB2. We used two siRNA oligonucleotides against RhoBTB2 (1 and 2) to determine any non-specific effects. Cells expressed the siRNA oligonucleotides for 72 hours before total RNA extraction. 10 samples have been analysed.

2008-10-25 | E-GEOD-8837 | biostudies-arrayexpress

An RNAi Screen for Skin Morphogenesis Unravels The Complexities of Rho GTPase Networks

Project description:An RNAi Screen for Skin Morphogenesis Unravels The Complexities of Rho GTPase Networks

| PRJNA507411 | ENA

Melanocyte precursors in the hair follicle bulge of repigmented vitiligo skin are controlled by RHO-GTPase, KCTD10 and CTNNB1 signaling

Project description:In repigmentation of human vitiligo, the melanocyte (MC) precursors in the hair follicle (HF) bulge proliferate, migrate and differentiate to repopulate the depigmented epidermis. Here we present a comprehensive characterization of pathways and signals in the bulge that control the repigmentation process. Using biopsies from vitiligo patients we have selectively harvested, by laser capture microdissection, MC and keratinocyte precursors from the HF bulge of untreated vitiligo skin and vitiligo skin treated with Narrow Band UVB (NBUVB). The captured material was subjected to whole transcriptome RNA sequencing. With this strategy, we found that repigmentation in the bulge MCs precursors is driven by KCTD10, a signal with unknown roles in the skin, and by CTNNB1 (encoding β-catenin) and RHO-GTPase (RHO), two signaling pathways previously shown to be involved in pigmentation biology.

2020-11-01 | GSE150954 | GEO

First Clinical Study Targeting ROR1, A Cancer Stem Cell Antigen Involved In Rho-GTPase Activation

Project description:First Clinical Study Targeting ROR1, A Cancer Stem Cell Antigen Involved In Rho-GTPase Activation

| PRJNA471247 | ENA