ARHGDIB
- Known as:
- ARHGDIB
- Catalog number:
- 001887A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ARHGDIB
Related genes to: ARHGDIB
- Gene:
- ARHGDIB NIH gene
- Name:
- Rho GDP dissociation inhibitor beta
- Previous symbol:
- RAP1GN1, GDIA2, GDID4
- Synonyms:
- Ly-GDI, RhoGDI2
- Chromosome:
- 12p12.3
- Locus Type:
- gene with protein product
- Date approved:
- 1994-08-29
- Date modifiied:
- 2016-04-01
Related products to: ARHGDIB
anti-ARHGDIB / D4 GDIAnti-ARHGDIB, Rabbit Polyclonal to ARHGDIB, Isotype , Host Rabbitanti-ARHGDIB, Rabbit polyclonal to ARHGDIB, Isotype IgG, Host RabbitAntibodies: ARHGDIB HOST: Goat Clonality: pAbAntigens ARHGDIB, 1-201aa, Human, GST tag, E.coli, RecombinantARHGAP9 Gene Rho GTPase activating protein 9ARHGDIB D4-GDI antibody Ab host: RabbitARHGDIB D4-GDI antibody Ab host: RabbitARHGDIB D4-GDI antibody Ab host: RabbitARHGDIB D4-GDI antibody Ab host: RabbitARHGDIB D4-GDI (cleavage specific) IgG2b antibody Ab host: MouseARHGDIB D4-GDI (cleaved) IgG2b antibody Ab host: MouseARHGDIB D4-GDI (N-term) antibody Ab host: GoatARHGDIB D4-GDI IgG antibody Ab host: MouseARHGDIB D4-GDI IgG1 antibody Ab host: Mouse Related articles to: ARHGDIB
- Whole-blood transcriptomic profiling can capture systemic immune-response alterations associated with COVID-19 and may support host-response-based classification. However, evidence regarding the discriminatory value of targeted immune-gene panels remains limited, and in small, high-dimensional datasets, the timing of feature selection may substantially affect model performance and interpretation. - Source: PubMed
Publication date: 2026/09/13
Yilmaz Zeynep BurcinKucukakcali ZeynepAkbulut Sami - Subcutaneous fat deposition critically impacts duck meat quality and feed efficiency. , a Rho GTPase regulator implicated in adipogenesis, remains functionally uncharacterized in poultry. - Source: PubMed
Publication date: 2026/03/20
Wang MingyuZheng HaoChen XingZhou Ao - The clinical relevance of non-HLA antibodies remains uncertain due to the lack of standardized assays. This study aimed to assess comparative reference values for non-HLA antibody profiles in a cohort of kidney transplant candidates on the deceased donor waiting list (WL group) with 0% calculated panel reactive antibodies (cPRA) and in healthy male blood donors (BD group). - Source: PubMed
Publication date: 2026/02/13
Quintiliano AAgrawal AZuccarelli MWakefield L LSchinstock C AGandhi M JBentall A J - Emerging evidence has highlighted lactylation as a critical link between metabolism and tumor progression. Through integrative lactylome and proteome profiling, we delineate the global landscape of protein lysine lactylation in bladder cancer, identifying lysine (K)47 and K50 of Rho guanosine diphosphate dissociation inhibitor β (ARHGDIB) as lactylation sites. Histone deacetylase (HDAC)2-mediated delactylation abrogates the tumor-suppressive function of ARHGDIB, promoting metastasis and cisplatin resistance of bladder cancer. Mechanistically, delactylation of ARHGDIB attenuates its binding affinity for Rac1, facilitating Rac1 membrane translocation and activation. This enhances DNA damage repair through the Rac1-MRN-ATM-CHK2 axis. Clinically, reduced ARHGDIB-K50 lactylation levels correlate with cisplatin resistance and poor prognosis. Entinostat, an inhibitor of class I HDAC, synergizes with cisplatin by preventing ARHGDIB delactylation. Collectively, our findings unveil a unique paradigm in which delactylation of tumor suppressors drives metastasis and chemoresistance. Targeting lactylation dynamics with HDAC inhibitors presents an avenue for intervention of bladder cancer. - Source: PubMed
Publication date: 2026/02/03
Xu GuanghuiLi YuqinPeng ShanZhao WeiXie TianleiZheng MinghaoWu ZhigangDeng YongmingFu YaoZhang ZhongqingZhang XuyuChen YijingShi JingyanChen WeiDing MengZhou YihuaDiao WenliGuo HongqianZhuang Junlong - RhoGDI2 is a RhoGTPase regulator that has roles in cytoskeleton organization and cell survival, amongst others. It is differentially expressed in many cell types and tissues, including several human cancers, where its expression has been correlated with either good or bad prognosis. To identify the underlying mechanisms, we knocked down its expression in human cancer cell lines. We observed that repression of RhoGDI2 expression, but not that of the closely related RhoGDI1, significantly reduces their proliferation rate. In parallel, RhoGDI2 suppression induces supernumerary centrosomes and inhibits ciliogenesis. As RhoGDIs are regulators of GTPases, we checked whether key RhoGTPases are involved in these effects. We found that silencing RhoA partially rescued the induction of supernumerary centrosomes and ciliary defects observed upon RhoGDI2 silencing. It was previously shown that RhoGDI2 is strongly expressed in immune cells and that there are striking similarities between primary cilia and immune synapses. Based on this knowledge, we silenced RhoGDI2 in NK cells and could demonstrate that this strongly affects their immune synapse-related cancer cell-killing activity. Altogether, these data suggest novel roles for RhoGDI2 in centrosome functions in human cancer and immune synapses in immune cells, which provides an explanation for its reported dual role in cancer. - Source: PubMed
Publication date: 2025/11/20
Tripathi MudrikaGarbacki NancyWillems JérômeCobraiville GaëlFillet MarianneColige AlainDeroanne Christophe F