Ask about this productRelated genes to: SLC30A8 antibody
- Gene:
- SLC30A8 NIH gene
- Name:
- solute carrier family 30 member 8
- Previous symbol:
- -
- Synonyms:
- ZnT-8, ZNT8
- Chromosome:
- 8q24.11
- Locus Type:
- gene with protein product
- Date approved:
- 2003-03-14
- Date modifiied:
- 2016-12-13
Related products to: SLC30A8 antibody
Related articles to: SLC30A8 antibody
- Type 2 diabetes (T2D) is a highly heritable, polygenic disease with over 600 loci identified through genome-wide association studies (GWAS). However, despite possessing unique genetic variation shaped by demographic history and admixture, Latin American populations remain markedly underrepresented in global genomic research. To address this gap, we conducted genome- and exome-wide analyses of 19,431 T2D cases and 105,611 controls from the Mexico City Prospective Study (MCPS). We identified 86 independent GWAS associations, including 21 novel signals, 15 of which replicated in external cohorts. Risk alleles at novel loci were enriched in individuals with Indigenous American ancestry. Exome analyses revealed rare and ultra-rare missense variants with substantial risk effects at and , as well as a protein-damaging variant in that reduced T2D risk by 45% in carriers. Integrative analyses indicate that T2D genetic architecture in Mexico is predominantly driven by common regulatory variation acting in the endocrine pancreas. Polygenic risk scores strongly stratified T2D risk and transferred to Indigenous Mexican populations. These findings demonstrate the power of large-scale genetic discovery in diverse populations to refine disease architecture and identify loci with potential therapeutic relevance. - Source: PubMed
Publication date: 2026/06/25
Torres Jason MBerumen JaimeAguilar-Ramirez DiegoTrichia EiriniBarajas-Olmos FranciscoGarcía-Ortiz HumbertoMorris SamTurner MichaelBarrera ElizabethLiu TianshuQuinto-Cortés Consuelo DPetty Lauren EGarcía-García LourdesTusié-Luna María TeresaAguilar-Salinas Carlos AChong Amanda YBaca PaulinaRivas FernandoBragg FionaGnatiuc Friedrichs LouisaHill Michael RHolland LisaVergara-Lope AlejandraWade RachelGaziano Michael JCollins RoryWheeler EleanorShuldiner Alan RBelow Jennifer ENorth Kari EPereira Alexandre CMoreno-Estrada AndrésOrozco LorenaAlegre-Díaz JesúsKuri-Morales PabloEmberson Jonathan RTapia-Conyer Roberto - The overlapping clinical features in young-onset type 2 diabetes (T2DM) present significant diagnostic difficulties. Variable autoimmunity and beta-cell dysfunction, which are related to the phenomenon, are not sufficiently consolidated to distinguish subclasses. - Source: PubMed
Publication date: 2026/04/25
Shil Kishore KumarHasan MashfiqulSultana NusratAbdus-Salam Sayad BinMahrukh HafsaFerdousi TahminaHasanat Muhammad Abul - Genome-wide association studies (GWAS) have identified numerous loci associated with Type 2 Diabetes (T2D), yet translating statistical signals into experimentally testable hypotheses remains a central challenge in post-GWAS biology. The predominance of non-coding regulatory variants complicates target gene assignment and raises uncertainty regarding optimal clustered regularly interspaced short palindromic repeats (CRISPR) perturbation strategy. Here, we present a structured CRISPR Actionability Framework that integrates genomic context, pancreatic islet enhancer overlap, tissue-specific expression validation, and locus clarity into a quantitative CRISPR Actionability Score (CAS). We applied this framework to ten genome-wide significant T2D loci and assigned modality-aware CRISPR strategies (knockout versus CRISPR interference). CAS values ranged from 4 to 10, enabling tiered prioritization into high, moderate, and lower experimental priority classes. High-priority loci included SLC30A8, TCF7L2, and KCNJ11, which demonstrated strong regulatory or coding evidence combined with islet expression support. By explicitly linking genomic architecture to perturbation modality, this framework provides a transparent and reproducible bridge between statistical genetics and functional genome editing. This approach establishes a scalable template for rational CRISPR target selection in complex disease research. - Source: PubMed
Publication date: 2026/06/16
Uddin Mohd MehboobKhan Syed Mohd Zakariya Ali - Detecting type 1 diabetes in presymptomatic stages is essential for therapies aimed at delaying clinical onset. - Source: PubMed
Winkler ChristianeFriedl NadineAbt RenateAckermann KathrinBently JuliaBraig SonjaBrämswig SusanneDunstheimer DesireeErmer UweEwald DominikGerstl Eva-MariaHammersen JohannaHaupt FlorianHergl MajaHubmann MichaelHummel SandraJochem BenediktKnopff AnnetteLange KarinLwowsky DominikNellen-Hellmuth NicolePrey BirgitRettner DanielaSchill SarahSchmidt SilkeScholz MarlonSindichakis MarinaStock JoannaStricker DominikVölkl Thomas M KWarncke KatharinaWeber LeonieWeiss AndreasBonifacio EzioAchenbach PeterZiegler Anette-Gabriele - The increasing prevalence of young-onset diabetes in Bangladesh presents a diagnostic challenge due to overlapping clinical phenotypes. Data regarding glutamic acid decarboxylase (GAD65) and, especially, Zinc Transporter 8 (ZnT8) antibodies in the Bangladeshi population remain scarce. - Source: PubMed
Rahman Md SaifurShadequl Islam A H MHosen MobarakAlam Mohammad JahangirSultana NusratHasan MashfiqulHasanat Muhammad Abul