CLEC16A (aa1040_53)
- Known as:
- CLEC16A (aa1040_53)
- Catalog number:
- Y214218
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- CLEC16A (aa1040_53)
Related genes to: CLEC16A (aa1040_53)
- Gene:
- CLEC16A NIH gene
- Name:
- C-type lectin domain containing 16A
- Previous symbol:
- KIAA0350
- Synonyms:
- Gop-1
- Chromosome:
- 16p13.13
- Locus Type:
- gene with protein product
- Date approved:
- 2006-08-25
- Date modifiied:
- 2017-03-23
Related products to: CLEC16A (aa1040_53)
Related articles to: CLEC16A (aa1040_53)
- CD4+ T cells harbor a disproportionate enrichment of immune disease risk loci and represent the primary cellular context for immune disease biology, yet the genes and regulatory programs these variants affect remain largely unknown. We combined targeted Perturb-seq of 1,032 -regulatory elements (CREs) overlapping 4,724 variants across 14 immune diseases with genome-wide Perturb-seq of all expressed genes in primary human CD4+ T cells, spanning 4.1 million cells. We identified 626 CRE-gene pairs, and connected CRE targets to downstream regulatory cascades. At the and /CLEC16A loci, we resolved target genes and linked noncoding variants to inflammatory and metabolic programs. Across diseases, we revealed that dispersed variants converged on shared and disease-specific programs. Our work provides a framework for tracing variant-to-CRE-to-gene-to-network in disease-relevant primary cells. - Source: PubMed
Publication date: 2026/03/11
Moonen Dewi P IClaringbould AnniqueGschwind Andreas RSchrod StefanBraunger JanaFeng ClaudiaRauscher BenediktYi JiaBi Shirley ZMatthess YvesKaulich ManuelAcob Ricelle AAyer ArunaEngreitz Jesse MVelten BrittaStegle OliverTrynka GosiaZaugg Judith BSchraivogel DanielSteinmetz Lars M - Epilepsy and thyroid cancer are prevalent disorders with distinct etiologies; however, emerging evidence suggests the presence of shared molecular mechanisms that remain largely unexplored. In this study, we aimed to identify and characterize common hub genes and potential diagnostic markers linking these two conditions using comprehensive in silico and in vitro approaches. Differentially expressed genes (DEGs) were analyzed from epilepsy datasets (GSE44456, GSE186334) and thyroid cancer datasets (GSE60542, GSE153659), leading to the identification of four shared hub genes: CD44, CALCOCO2, ALDH4A1, and CLEC16A. Expression validation using RT-qPCR confirmed consistent patterns, with CD44 and CLEC16A significantly upregulated and CALCOCO2 and ALDH4A1 downregulated in disease cell lines compared to controls. Receiver operating characteristic (ROC) curve analysis demonstrated strong diagnostic potential for these genes in both diseases, with area under the curve (AUC) values exceeding 0.90. Functional enrichment and pathway analyses revealed that these genes are involved in oncogenic signaling, immune regulation, and tumor progression. Genetic alteration analysis indicated frequent mutations and copy number variations, while promoter methylation profiling suggested epigenetic regulation associated with disease outcomes. Survival analysis further identified ALDH4A1 and CLEC16A as prognostic markers. Moreover, in vitro and in vivo experiments demonstrated that CD44 and CLEC16A regulate cellular proliferation, migration, and clonogenicity through extracellular matrix (ECM)-receptor interactions involving CCL5, STAT3, CXCR4, and RAC1 signaling pathways. Collectively, these findings provide new insights into the shared molecular landscape of epilepsy and thyroid cancer, highlighting potential diagnostic biomarkers and therapeutic targets. - Source: PubMed
Publication date: 2026/04/08
Wang Si YingLiu TianyuZhang DechunLiu WeixuanQian MengLi RongfangYu Liu ZhenWu Pei - Hypertension is an important target for primordial prevention of complex, noncommunicable diseases, and its prevalence remains high across populations. The urban population in India is at a high risk of hypertension, but the genetic basis of hypertension in this population remains poorly understood. - Source: PubMed
Publication date: 2026/03/22
Kanaskar SamikaPatel Ashwini AJaisinghani Manisha TPipal Kanchan VKanaskar MangeshMamtani ManjuKulkarni Hemant - Nephrotic syndrome (NS), a common glomerular disease in children, is classified based on response to corticosteroid therapy as either steroid-sensitive nephrotic syndrome (SSNS), or steroid-resistant nephrotic syndrome (SRNS). However, there are no current reliable predictors of therapy response at initial clinical presentation. - Source: PubMed
Publication date: 2026/02/24
Tu TiffanyOchoa AlejandroSood AmikaDabrik AshleyChryst-Stangl MeganLane BrandonWu GuanghongDonovan FrankHarper UrsulaChandrasekharappa SettaraEsezobor ChristopherSolarin AdaobiHooper DavidSethna ChristineAmaral SandraKallash MahmoudRheault MichelleVerghese PriyaDharnidharka VikasSalmon EloiseWeng PatriciaSrivastava TarakSeifert Michael EPruette CozumelSelewski DavidGibson KeishaHunley TracyAbeyagunawardena AsiriThalgahagoda ShenalBagga ArvindSinha AditiWebb NicholasGreenbaum LarryGharavi AliKiryluk KrzysztofKretzler MatthiasGuay-Woodford LisaSanna-Cherchi SimoneBierzynska AgnieszkaKoziell AniaWelsh GavinSaleem MoinRotimi CharlesChambers EileenChan Cliburn Jackson AnnetteAdeyemo AdebowaleGbadegesin Rasheed - Hematopoietic stem and progenitor cells (HSPCs) arise from hemogenic endothelium via the endothelial-to-hematopoietic transition (EHT), a process requiring precise mitochondrial quality control. Here, we identify Clec16a, an E3 ubiquitin ligase, as a conserved regulator of embryonic HSPC emergence. In zebrafish and HEK293T models, Clec16a is enriched in hemogenic endothelium, and its loss disrupts arterial identity, impairs EHT, and reduces lymphoid, erythroid, and myeloid lineages. Transcriptomic and proteomic analyses show that Clec16a deficiency compromises mitophagy by promoting aberrant K48-linked ubiquitination and proteasomal degradation of ATG5, leading to mitochondrial dysfunction and elevated reactive oxygen species. These findings establish Clec16a as an essential regulator linking ubiquitin signaling, mitophagy, and hematopoietic fate specification. Our study defines a mitophagy-dependent checkpoint that safeguards mitochondrial homeostasis during developmental hematopoiesis and provides insight into the metabolic control of hematopoietic disorders. - Source: PubMed
Publication date: 2026/02/19
Cai ShuyangZhang QianLuo QianLi HonghuTao YuchenFeng CongTie RuxiuZeng XiangjunChen ShuoSong ZijunWang AnliHu QiBao JizhangSu YangChen YirongXu HaoHu KexinDing NingNi RunfengJin RuiWu FanLi XiaojingYang XinyiXu YangHuang HeLu Jiahui