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
- This study presents an in-depth analysis of an interactome comprising approximately 1033 nodes, focusing on its topology, reliability, and functional implications, with particular attention to the small mitochondrial proteins of the Humanin family and their nuclear-encoded MTRNR2Lx paralogs. The analysis, conducted through stringent high-reliability filters and experimentally supported interaction data, produced a curated network model in which approximately 70% of the retained interactions were supported by experimental evidence, providing a solid basis for network-based functional interpretation. The topology of the interactome showed scale-free and modular network characteristics, with hub and bottleneck nodes defining highly connected stress-response and regulatory modules. Humanin-related proteins, positioned at the periphery of the interactome, emerged as candidate modulatory nodes linking peripheral signaling interfaces to broader functional modules. Mitochondrial Humanin may contribute to early cytoprotective responses, including pathways associated with BAX-dependent apoptosis regulation, whereas nuclear MTRNR2Lx proteins appear to be connected to more sustained regulatory networks involving neuroprotection- and apoptosis-associated modules under chronic stress conditions. In particular, the MTRNR2Lx-FPR2/G-protein module, including GNB1, emerged as a candidate signaling interface that may contribute to the downstream organization of Humanin-related responses. This network-based distinction supports the view that Humanin-family peptides may operate as modulators of stress-response networks rather than as isolated effectors of intrinsic mitochondrial functions. Overall, the methodological approach, results, and proposed model provide new insights into the systems-level organization of Humanin biology and identify prioritized molecular candidates for future in vitro and in vivo validation in the context of neurodegeneration, apoptosis, and cellular stress. - Source: PubMed
Publication date: 2026/07/03
Shahzaib MohdAprile DomenicoLaporta GianluigiGalderisi UmbertoColonna Giovanni - Tooth agenesis is a genetically heterogeneous developmental anomaly in which disturbances of morphogen signaling, cytoskeletal organization, and mineralization converge during odontogenesis. Building on a previously published clinical and exome study of two Lebanese families with familial nonsyndromic tooth agenesis that identified rare segregating missense variants in trio Rho guanine nucleotide exchange factor (TRIO) and calcium voltage-gated channel auxiliary subunit alpha2delta 2 (CACNA2D2), this work examines how these genes may participate in a shared mechanistic axis during human tooth development. - Source: PubMed
Publication date: 2026/05/25
Nabbout FideleSabbagh JosephEl Hajj JoelleGhassibe Michella - Childhood-onset dystonia (COD) encompasses a clinically and etiologically heterogeneous group of disorders, often with overlapping features. Genetic testing plays a pivotal role in uncovering underlying causes, identifying treatable subtypes, and informing individualized management strategies. - Source: PubMed
Publication date: 2026/06/16
Yilmaz SanemSerdaroglu EsraSimsek ErdemKara BulentTurkdogan DilsadYis UlucErol IlknurYuksel DenizKanmaz SedaEroglu ArzuCanpolat MehmetKomur MustafaCıtak Kurt NeseSakarya Gunes AyferSoydemir DidemBesen SeydaBektas OmerKirik SerkanAtalay Celik HaleArdicli DidemAksoy AyseYarar CoskunCerci Kubur CisilOlgac Dundar NihalGungor OlcayKamasak TulayOlculu Cemile BusraGumus HakanYildirim MiracIsik EsraAtik TahirCogulu OzgurBasak Ayse NazliSunnetci Akkoyunlu DenizÖzbakır Derya HazalKayhan GülsümGerik Çelebi Hamide BetulKaraer KadriDundar MunisKaiyrzhanov RauanCeylaner SerdarPer HuseyinHiz Ayse SemraCansu AliOkuyaz CetinAnlar BanuTekgul Hasan - Microalgal protein (MP, Spirulina) is a highly promising novel sustainable protein resource, yet the mechanisms by which it regulates the production performance and milk quality of lactating dairy cows remain unclear. This study elucidates the regulatory mechanisms by which amino acid balancing and MP supplementation modulate production performance and milk quality in mid-lactation dairy cows fed low-protein diet (LPD). Results demonstrated that dietary interventions significantly altered milk composition. To elucidate the underlying molecular mechanisms, proteomic and metabolomic analyses were employed, leading to the identification of 1186 differentially expressed proteins (DEPs) and 1167 differentially expressed metabolites (DEMs). Key signaling molecules, such as GNB1, GNG5, GNG10, and GRB2, interacted with metabolic hubs like α-ketoglutaric acid/Glutamic acid within a regulatory network, enhancing amino acid sensing and signal transduction. The observed coordinated changes in key signaling molecules and metabolic hubs suggest that amino acid sensing and signal transduction pathways may be activated, potentially promoting energy metabolism and nitrogen conversion efficiency. The identified key molecular markers of milk quality lay a scientific basis for the production of high-quality dairy raw materials and the development of value-added dairy products. - Source: PubMed
Publication date: 2026/06/16
He TianleRen WenyiYang ShuangmingBai JinniGuo YajunWu YongjiangShi JinpingYue Caijuan - -related neurodevelopmental disorder is a rare developmental encephalopathy caused by pathogenic variants in The disorder presents with early-onset developmental delay, hypotonia, movement disorders, seizures and/or epilepsy and varied electroencephalographic (EEG) findings, which may occur even in the absence of seizures.We report a male toddler with early-onset global developmental delay, hypotonia, dysmorphic features, bilateral sensorineural hearing loss, nystagmus, transient neonatal focal seizures and emerging EEG findings. Genetic testing identified a pathogenic missense variant NM_002074.5:c239T>A (p.Ile80Asn) inherited from an asymptomatic father with mosaicism.This case illustrates the clinical variability of GNB1 encephalopathy, expands the spectrum of reported inheritance patterns and highlights the importance of early genetic testing of infants with developmental delay and pathological EEG patterns. Recognition of the electroclinical patterns is essential for early diagnosis, genetic counselling and multidisciplinary management. The future expansion of longitudinal clinical and EEG data will be essential for prognosis and possible future therapeutic approaches. - Source: PubMed
Publication date: 2026/05/19
Alili Ademi LeartaSukarova-Angelovska ENonkulovski DaniloAdemi Blerim