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The interactome of G3BP1 in UMUC3 cells

ABSTRACT: The HA-tagged G3BP1 complex was obtained by co-IP with anti-HA antibodies from UMUC3 cells stably expressing HA-tagged G3BP1. The purified immunoprecipitants were resolved on gradient SDS-PAGE, silver-stained, and subjected to MS analysis.

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Cell Culture, Bladder Urothelial Cell

DISEASE(S): Bladder Transitional Cell Papilloma

SUBMITTER: Jiawei Chen

LAB HEAD: Jiawei Chen

PROVIDER: PXD035722 | Pride | 2024-05-23

REPOSITORIES: Pride

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Dataset's files

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			Action	DRS
	R20210901912_UMUC_G3IP.msf	Msf
	R20210901912_UMUC_G3IP.raw	Raw
	R20210901912_UMUC_IGG.msf	Msf
	R20210901912_UMUC_IGG.raw	Raw

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Publications

G3BP1 and SLU7 Jointly Promote Immune Evasion by Downregulating MHC-I via PI3K/Akt Activation in Bladder Cancer.

Zheng Xianchong X Chen Jiawei J Deng Minhua M Ning Kang K Peng Yulu Y Liu Zhenhua Z Li Xiangdong X Zhou Zhaohui Z Tang Huancheng H Li Yaoying Y Kang Tiebang T Liu Zhuowei Z

Advanced science (Weinheim, Baden-Wurttemberg, Germany) 20231212 7

Immune checkpoint inhibitors (ICIs) show promise as second-line treatment for advanced bladder cancer (BLCA); however, their responsiveness is limited by the immune evasion mechanisms in tumor cells. This study conduct a Cox regression analysis to screen mRNA-binding proteins and reveals an association between Ras GTPase-activating protein-binding protein 1 (G3BP1) and diminished effectiveness of ICI therapy in patients with advanced BLCA. Subsequent investigation demonstrates that G3BP1 enhance ...[more]

PMID: 38084438

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G3BP1 translocates into mitochondria to impair MCU complex function and promotes NASH progression [G3bp1-HKO and G3bp1-Flox mice with BSA or PA treatment]

Project description:Mitochondrial calcium signaling plays a critical role in mitochondrial homeostasis during non-alcoholic steatohepatitis (NASH) progression. Here, we report Ras‐GTPase activating protein SH3 domain‐binding protein 1 (G3BP1), a core protein of stress granule (SG), significantly upregulated in NAFLD/NASH patients, mouse models and palmitic acid-stimulated hepatocytes. Hepatocyte-specific G3BP1 deficiency attenuates NASH in two dietary mouse models. SG and the mitochondrial import protein TOM70 collaboratively mediate the translocation of G3BP1 to the mitochondria. G3BP1 interacts and stabilizes mitochondrial calcium uptake 1 (MICU1) via inhibiting YME1L1-mediated degradation of MICU1, and also impedes MCU complex activity and assembly, leading to mitochondrial calcium overload. Moreover, metabolic stress suppresses TRIM25-mediated K63-ubiquitination of G3BP1 and subsequent SG disassembly. Pharmacological inhibition of G3BP1 impairs the G3BP1-MICU1 interaction and prevents mitochondrial homeostasis imbalance and NASH progression. Collectively, we uncover the significant role of mitochondrial G3BP1 in mitochondrial homeostasis and NASH progression, which provides a potential target for therapeutic interventions.

2024-08-18 | GSE274650 | GEO

G3BP1 Binds to Guanine Quadruplexes in mRNAs

Project description:we identify G3BP1 as a novel rG4-binding protein, and reveal that G3BP1 can modulate mRNA stability through its binding with rG4 structures

2021-03-16 | GSE168943 | GEO

ChIP-seq analysis of G3BP1 in KGN cells

Project description:To investigate whether G3BP1 binds to telomeric DNA, we performed the ChIP-seq analysis of G3BP1 in KGN cells.

2024-04-14 | GSE263539 | GEO

G3BP1 inhibits Cul3SPOP to amplify AR signaling and promote prostate tumorigenesis

Project description:Speckle-type POZ protein (SPOP), an E3 ubiquitin ligase, acts as a tumor suppressor. We identified G3BP1 as non-substrate interactor of SPOP. G3BP1 is a well-known oncogene in many cancer types, but its role in prostate cancer (PCa) remains largely elusive. We showed that G3BP1 functions as an upstream regulator and potent endogenous inhibitor of Cul3SPOP, suggesting a distinctive Cul3SPOP inactivation independent of SPOP mutations. Transcriptomic analysis together with functional studies revealed that the G3BP1-SPOP ubiquitin signaling axis is involved in PCa progression through activating AR signaling. Further, AR upregulates G3BP1 to potentiate feed-forward amplification of signaling through G3BP1-SPOP axis. Overall, we show G3BP1high PCa tumors constitute a new subset where G3BP1 inhibits Cul3SPOP function to upregulate AR signaling, and promotes tumorigenesis.

2021-09-26 | GSE138612 | GEO

G3bp1-miR-1 axis regulates cardiomyocyte hypertrophy

Project description:We examine the role of G3bp1, a RNA binding protein and site specific endoribonuclease in gene expression in isolated neonatal cardiomyocytes. RNAseq data from cardiomyocytes were infected with adenoviruses expressing shRNA against G3bp1 (ad-siG3bp1) or Luciferase (ad-siLUC, control) showed significant decrease in transcript abudnnace of cardiac-enriched genes involved in Calcium handling, contraction, action potential and sacromere function. On the other hand increase was observed in genes that regulate Hippo, TNF and TGFb signaling. Knockdown of G3bp1 inhibited endothelin-1 induced cardiomyocyte hypertrophy.

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G3BP1 translocates into mitochondria to impair MCU complex function and promotes NASH progression

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RAN directly binds and stabilizes G3BP1 mRNA in the nucleus to facilitate proliferation and metastasis of nasopharyngeal carcinoma (si-G3BP1 RNA-seq)

Project description:RNA binding proteins (RBPs) play a critical role in tumor progression by participating in the post-transcriptional regulation of RNA. However, the expression and function of RBPs in nasopharyngeal carcinoma (NPC) remain elusive. This study identified 5 RBPs (RAN, EZH2, RDM1, HRSP12, and ALYREF) that were up-regulated in NPC and could promote NPC cells migration or proliferation. RAN was first investigated because of its most significant effect on NPC cells. Functionally, RAN facilitated NPC proliferation, migration, and invasion in vitro and in vivo. High expression of RAN was associated with poor prognosis of NPC patients and could be performed as a prognostic biomarker. Mechanistically, RAN mediated the nucleus import of TDP43 and enhanced TDP43 nuclear distribution. On the other hand, RAN was directly bound to the coding sequence of G3BP1 mRNA and served as an adapter to facilitate TDP43 interacting with G3BP1 mRNA 3’untranslated region. Thereby increased G3BP1 mRNA stability in the nucleus and led to up-regulation of G3BP1, which further enhanced ATK/ERK phosphorylation and ultimately promoted NPC proliferation and metastasis.

2024-10-31 | GSE262032 | GEO

Huntington’s disease mice and human brain tissue exhibit increased G3BP1 granules and TDP43 mislocalization

Project description:We identify cerebrospinal fluid extracellular vesicle miRNAs in Huntington’s Disease that are enriched for targeting G3BP1 and show aberrant G3BP1 granule dynamics in HD mice and human brain tissue.

2021-05-07 | GSE173546 | GEO

LIMK2 promotes melanoma tumor growth and metastasis through G3BP1-ESM1 pathway-mediated apoptosis inhibition

Project description:Melanoma is the leading cause of skin cancer-related deaths, and current melanoma therapies, including targeted therapies and immunotherapies, benefit only a subset of metastatic melanoma patients due to either intrinsic or acquired resistance. LIM domain kinase 2 (LIMK2) is a serine/threonine kinase that plays an important role in the regulation of actin filament dynamics. Here, we show that LIMK2 is overexpressed in melanoma, and its genetic or pharmacological inhibition impairs melanoma tumor growth and metastasis in both cell culture and mice. To determine the mechanism by which LIMK2 promotes melanoma tumor growth and metastatic progression, we performed a phosphoproteomics analysis and identified G3BP1 as a key LIMK2 target, which mirrored the effects of LIMK2 inhibition when inhibited. To further determine the role of G3BP1 downstream of LIMK2, we knocked down the expression of G3BP1, performed RNA-seq analysis, and identified ESM1 as a downstream target of G3BP1. G3BP1 was required for ESM1 mRNA stability, and ESM1 ectopic expression rescued LIMK2 or G3BP1 inhibition-induced suppression of melanoma growth and metastatic attributes. These results collectively identify the LIMK2→G3BP1→ESM1 pathway as a facilitator of melanoma tumor growth and metastasis and document that LIMK2 is a therapeutically tractable target for melanoma therapy.

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G3BP1-linked mRNA partitioning supports selective protein synthesis in response to oxidative stress

Project description:Cells limit energy-consuming mRNA translation during stress to maintain metabolic homeostasis. Sequestration of mRNAs by RNA binding proteins (RBPs) into stress granules (SGs) reduces translation, but it remains unclear whether SGs also function in partitioning of specific transcripts to polysomes (PSs) to guide selective translation and stress-adaptation in cancer. Transcripts enriched in PSs, defined by polysome fractionation and RNAseq, were compared with mRNAs complexed with the SG-nucleator protein, G3BP1, defined by spatially-restricted enzymatic tagging. Short-term oxidative stress profoundly altered mRNA translation by promoting selective enrichment of transcripts within SGs or PSs. G3BP1 participates in this compartmentalisation by sequestering transcripts in SGs. Under stress, G3BP1-bound transcripts are PS-depleted and encode proteins involved in mRNA translation, pro-apoptosis, and mitochondrial function. In contrast, specific PS-enriched transcripts disassociate from G3BP1 under stress to encode proteins involved in diverse cellular cytoprotective pathways. Therefore, G3BP1 partitioning guides selective translation to support stress adaptation and cell survival.

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