CLEC16A

Last update 08 May 2025

Basic Info

Synonyms

C-type lectin domain containing 16A, C-type lectin domain family 16 member A, CLEC16A

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Introduction

Regulator of mitophagy through the upstream regulation of the RNF41/NRDP1-PRKN pathway. Mitophagy is a selective form of autophagy necessary for mitochondrial quality control. The RNF41/NRDP1-PRKN pathway regulates autophagosome-lysosome fusion during late mitophagy. May protect RNF41/NRDP1 from proteasomal degradation, RNF41/NRDP1 which regulates proteasomal degradation of PRKN. Plays a key role in beta cells functions by regulating mitophagy/autophagy and mitochondrial health.

100 Clinical Results associated with CLEC16A

100 Translational Medicine associated with CLEC16A

0 Patents (Medical) associated with CLEC16A

158

Literatures (Medical) associated with CLEC16A

01 Mar 2025·Nature Neuroscience

CLEC16A in astrocytes promotes mitophagy and limits pathology in a multiple sclerosis mouse model

Article

Author: Klement, Wendy ; Zandee, Stephanie E J ; Mahler, Joao V ; Soleimanpour, Scott A ; Li, Zhaorong ; Srun, Lena ; Chao, Chun-Cheih ; Rothhammer, Veit ; Wheeler, Michael A ; Lee, Hong-Gyun ; Prat, Alexandre ; Quintana, Francisco J ; Lee, Joon-Hyuk ; Neel, Dylan ; Chiu, Isaac ; Andersen, Brian M ; Bergstresser, Matthew ; Basu, Himanish ; Lipof, Gabriel ; Khurana, Vikram ; Kadowaki, Atsushi ; Ndayisaba, Alain ; Illouz, Tomer

Astrocytes promote neuroinflammation and neurodegeneration in multiple sclerosis (MS) through cell-intrinsic activities and their ability to recruit and activate other cell types. In a genome-wide CRISPR-based forward genetic screen investigating regulators of astrocyte proinflammatory responses, we identified the C-type lectin domain-containing 16A gene (CLEC16A), linked to MS susceptibility, as a suppressor of nuclear factor-κB (NF-κB) signaling. Gene and small-molecule perturbation studies in mouse primary and human embryonic stem cell-derived astrocytes in combination with multiomic analyses established that CLEC16A promotes mitophagy, limiting mitochondrial dysfunction and the accumulation of mitochondrial products that activate NF-κB, the NLRP3 inflammasome and gasdermin D. Astrocyte-specific Clec16a inactivation increased NF-κB, NLRP3 and gasdermin D activation in vivo, worsening experimental autoimmune encephalomyelitis, a mouse model of MS. Moreover, we detected disrupted mitophagic capacity and gasdermin D activation in astrocytes in samples from individuals with MS. These findings identify CLEC16A as a suppressor of astrocyte pathological responses and a candidate therapeutic target in MS.

01 Feb 2025·Heliyon

The stage- and subgroup-specific impact of non-HLA polymorphisms on preclinical type 1 diabetes progression

Article

Author: Desouter, Aster K ; Gorus, Frans K ; Van der Auwera, Bart J ; Chapaza, Kaven B ; Lapauw, Bruno ; Lebrethon, Marie-Christine ; Abrams, Pascale ; Keymeulen, Bart ; Nobels, Frank ; Van de Casteele, Mark ; Vandewalle, Julie

Besides variation within the HLA gene complex determining a major part of genetic susceptibility to Type 1 diabetes, genome-wide association studies have identified over 60 non-HLA loci also contributing to disease risk. While individual single nucleotide polymorphisms (SNPs) have limited predictive power, genetic risk scores (GRS) can identify at-risk individuals. However, current models do not fully capture the heterogeneous progression of asymptomatic islet autoimmunity, especially in autoantibody-positive subjects. In this study, we investigated the additional stage-specific impact of 17 non-HLA loci on previously established prediction models in 448 persistently autoantibody-positive first-degree relatives. Cox regression and Kaplan Meier survival analysis were used to assess their influence on progression from single to multiple autoantibody-positivity, and from there to clinical onset. FUT2 and CTSH significantly accelerated progression of single to multiple autoAb-positivity, but only in presence of insulin autoantibodies and HLA-DQ2/DQ8, respectively. At the stage of multiple autoantibody-positivity, progression to clinical onset was impacted by various non-HLA SNPs either as independent predictors (GLIS3, CENPW, IL2, GSDM, MEG3A, and NRP-1) or through interaction with HLA class I alleles (CLEC16A, NRP-1, TCF7L2), maternal diabetes status (CTSH), or a high-risk autoantibody-profile (CD226). Our data indicate that, unlike for GRS, the weight of distinct non-HLA polymorphisms varies significantly among individuals at risk, depending on disease stage and other stage-specific risk factors. They refine our previous stage-specific prediction models including age, autoantibody-profile, HLA genotype, and other non-HLA SNPs, and emphasize the importance of stratifying accordingly to personalize time-to-event prediction in risk groups, or for preparing or interpreting prevention trials.

01 Nov 2024·Journal of Human Genetics

Genomic variants associated with age at diagnosis of childhood-onset type 1 diabetes

Article

Author: Bougnères, Pierre ; Perge, Kevin ; Le Fur, Sophie ; Lathrop, Mark ; Belot, Marie-Pierre ; Mai, Thanh-Nga ; Kamatani, Yoichiro ; Valleron, Alain-Jacques ; Shao, XiaoJian

Age at diagnosis (AAD) of Type 1 diabetes (T1D) is determined by the age at onset of the autoimmune attack and by the rate of beta cell destruction that follows. Twin studies found that T1D AAD is strongly influenced by genetics, notably in young children. In young UK, Finnish, Sardinian patients AAD-associated genomic variants were previously identified, which may vary across populations and with time. In 1956 children of European ancestry born in mainland France in 1980-2008 who declared T1D before 15 years, we tested 94 T1D-associated SNPs for their association with AAD using nonparametric Kruskal-Wallis test. While high-risk HLA genotypes were not found to be associated with AAD, fourteen SNPs located in 12 non-HLA loci showed a strong association (2.9 × 10^-12 < P < 1.4 × 10^-3 after FDR correction). Four of these loci have been associated with AAD in previous cohorts (GSDMB, IL2, TNFAIP3, IL1), supporting a partially shared genetic influence on AAD of T1D in the studied European populations. In contrast, the association of 8 new loci CLEC16A, TYK2, ERBB3, CCR7, FCRL3, DNAH2, FGF3/4, and HPSE2 with AAD is novel. The 12 protein-coding genes located within these loci are involved in major immune pathways or in predisposition to other autoimmune diseases, which suggests a prominent role for these genes in the early immune mechanisms of beta cell destruction.

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CLEC16A

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