Ask about this productRelated genes to: GNB1 antibody
- Gene:
- GNB1 NIH gene
- Name:
- G protein subunit beta 1
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 1p36.33
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2017-04-12
Related products to: GNB1 antibody
Related articles to: GNB1 antibody
- Multiple genetic variants of specific genes, such as KIT, GNAI2, and SETD2, have been reported in canine mast cell tumors (MCTs). A familiar internal tandem duplication of KIT in exon 11 is associated with poor prognosis. However, others common mutated genes in canine MCTs as increased risks to recurrence or death remain unexplored. This study investigated 39 genetic variants contributed to MCT-related risk factors and prognoses in paraffin shaved specimens from 38 low-grade and 34 high-grade MCTs using multiplex genotyping (MassARRAY, Agena Bioscience). The associations between observed genetic variants and prognostic factors were statistically analyzed. SETD2 c.1108_1109del tended to present in MCTs with aberrant expression of KIT (P = 0.05). GNB1 c.346_347delinsTA/TT wild types were likely to harbor in less aggressive MCTs (P = 0.007). MCT dogs having TP53 c.659 T > C were 1.65 times higher hazard risk on decreased time to recurrence by univariate analysis (95% CI 1.02-2.67, P = 0.041), but not in multivariate analysis. Our study suggests that SETD2 c.1108_1109del, and TP53 c.659 T > C may associate with poor prognosis; however, further study with larger samples is needed to confirm these correlations. - Source: PubMed
Publication date: 2026/03/04
Sirivisoot SirintraKasantikul TanitTechangamsuwan SompornRungsipipat Anudep - - Source: PubMed
Huang CaiqiangLi RunguangYang ChangshengDing RuiLi QingchuXie DenghuiZhang RongkaiQiu Yiyan - Clinical manifestations of 1p36.33 duplications vary depending on duplication size. This region is prone to copy number variants associated with diverse phenotypes. We report a novel 1p36.33p36.32 duplication in a patient with developmental delay and facial dysmorphism. The causative duplication was detected by whole-genome Oligo-array CGH and confirmed by real-time PCR. Integrative bioinformatic analyses-including network analysis, phenotype-driven gene prioritisation, and dosage sensitivity assessment-were performed to explore the molecular basis of the phenotype; we used integrative bioinformatic analyses, including network analysis, phenotype-driven gene prioritisation, and dosage sensitivity assessment. Assessment of a child with tonic seizures, developmental delay, and dysmorphic facial traits revealed a 2.3 MB gain in the 1p36.33p36.32 region (nucleotide 898,721 to 3,153,945) through array CGH. Bioinformatic analyses identified several candidate genes, including GABRD, DVL1, and GNB1, which are implicated in neurodevelopmental and congenital disorders. Pathway enrichment analysis revealed significant involvement of the '1P36 Copy Number Variation Syndrome' pathway. This case expands the phenotypic spectrum of 1p36 duplications and highlights the importance of integrating clinical, genomic, and bioinformatic data for accurate interpretation. - Source: PubMed
Eslahi AtiehKahaei Mir SalarShirvan Bita BarazandehAlerasool MasoomeTabarestani SepidehRezaie RazieHashemi NargesAkhondian JavadArabi MobinaEbrahimzadeh FarnooshToosi Mehran BeiraghiMojarrad Majid - Prostate cancer (PCa) is the most prevalent malignancy among men worldwide. Advanced prostate cancer is characterized by aggressive progression, limited therapeutic response, and poor prognosis. Elucidating its oncogenic mechanisms may provide new opportunities for targeted intervention. Increasing evidence suggests that modulating cytoprotective autophagy represents a promising strategy for improving cancer treatment efficacy and overcoming drug resistance. Here, we identified the G protein subunit GNG4 as a crucial regulator of prostate cancer development. GNG4 expression was markedly elevated in advanced prostate cancer phenotypes and positively correlated with tumor survival, apoptosis, and migration. Further analysis demonstrated that GNG4 depletion suppressed autophagy and enhanced cellular sensitivity to enzalutamide. Mechanistically, GNG4 interacts with GNB1 to stabilize the downstream effector protein GNAI3 through the ubiquitination-proteasome pathway. These three distinct G protein subunits form a functional complex that regulates intracellular autophagy and subsequently influences the malignant behavior of prostate cancer. Furthermore, inhibition of autophagy or GNG4 knockdown significantly increased the antitumor efficacy of enzalutamide both in vitro and in vivo. Our findings identified GNG4 as a pivotal modulator of prostate cancer progression and proposed it as a promising therapeutic target to enhance the clinical response to enzalutamide. GNG4 interacts with GNB1 to stabilize GNAI3 via the ubiquitination-proteasome pathway, thereby activating autophagy. This process promotes prostate cancer progression and resistance to androgen receptor signaling inhibitors (ARSis). In contrast, GNG4 knockdown or pharmacological inhibition of autophagy restores ARSI sensitivity and suppresses tumor growth. - Source: PubMed
Publication date: 2026/01/28
Chen LeiZhang JingyanHu YanshuoPeng XufengWang HongChen BinghuaXia JunXue WeiPan Chun-Wu - Developmental language disorders (DLDs) are common neurodevelopmental conditions, affecting approximately 7-10% of children, with significant impacts on communication, academic achievement, and social integration. While genetic factors are known contributors, the underlying genomic architecture and biological pathways remain incompletely understood. This analysis explores key genomic biomarkers of DLD and investigates their functional interactions. - Source: PubMed
Adnan Hassan RafalAl-Fatlawi Ali