anti-C-Type Lectin Domain Family 16, Member A (CLEC16A) Antibodies

Human C-Type Lectin Domain Family 16, Member A (CLEC16A) interaction partners

1. The genotypes of IL-4 (rs2243250)*C/C and CLEC16A (rs6498169)*G/G were associated with primary progressive multiple sclerosis in Russians. The association between the HLA-DRB1*15 and PPMS found out in other populations was confirmed in Russians.

2. Data (including data from studies using knockout and transgenic mice/cells) suggest that CLEC16A, NRDP1, and USP8 form tripartite complex; CLEC16A-NRDP1-USP8 complex appears to rely on ubiquitin signals to promote mitophagy and maintain mitochondrial function necessary for beta-cell function. (CLEC16A = C-type lectin domain family 16 member A; NRDP1 = ubiquitin-protein ligase NRDP1; USP8 = ubiquitin specific peptidase 8)

3. Golgi-associated CLEC16A negatively regulates autophagy via modulation of mTOR activity.

4. Study provides evidence that Clec16a plays a key role in the survival of Purkinje cells and in the degradative function or clearance of autolysosomes.

5. A possible regulatory role for the multiple sclerosis-associated rs12927355 in CLEC16A.

6. CLEC16A was found to be a susceptibility factor for SLE, with possible contribution to the development of the disease.

7. Clec16a knockdown mice showed reduced number of B cells and elevated IgM levels compared with controls.

8. identify CLEC16A as a pivotal gene in multiple sclerosis that serves as a direct regulator of the human leukocyte antigen class II pathway in antigen-presenting cells.

9. data suggests that two polymorphisms of the CLEC16A gene play an important role in the developing of ACS in men.

10. This study demonstrated that the Polymorphism, Single Nucleotide of CLEC16A is associated with multiple sclerosis in Russia.

11. The study suggested that a CLEC16A polymorphism may be protective against Vogt-Koyanagi-Harada syndrome syndrome in a Chinese Han population.

12. Our results suggest that polymorphisms rs6498169 of CLEC16A gene confers susceptibility to AITDs. We therefore disclose for the first time the association of rs6498169 SNP with AITDs.

13. Forty-eight SNPs, all located in CLEC16A, provided a statistically significant association with type 1 diabetes mellitus, with rs34306440 being most significantly associated. The mechanisim is likely through reduced expression of DEXI transcripts.

14. Study demonstrates that a diabetogenic SNP in the CLEC16A locus correlates with islet CLEC16A expression, beta cell function, and glycemic control in human subjects. Clec16a controls beta cell function and prevents diabetes by controlling mitophagy.

15. The data indicates a possible regulatory role for multiple sclerosis-associated non-coding CLEC16A SNPs and a common control mechanism for the expression of CLEC16A, SOCS1 and DEXI.

16. Polymorphisms in the inflammatory genes CIITA, CLEC16A and IFNG influence BMD, bone loss and fracture in elderly women

17. Genome-wide significant association was found for rs20541 and rs998592, thus establishing IL-13 and KIAA0350/CLEC16A as susceptibility loci for alopecia areata. IL-13 and KIAA0350/CLEC16A are also susceptibility loci for other autoimmune diseases.

18. Fine mapping identified 26 single-nucleotide polymorphisms (SNPs) across the CLEC16A-SOCS1 and 11 SNPs across the SPIB locus with significant association to primary biliary cirrhosis.

19. A significant association with multiple sclerosis is found for four single nucleotide polymorphisms within the CLEC16A gene, all located in the same linkage disequilibrium (LD) block.

20. Data show independent genetic signals in the CIITA-CLEC16A-SOCS1 gene complex in multiple sclerosis susceptibility.

Mouse (Murine) C-Type Lectin Domain Family 16, Member A (CLEC16A) interaction partners

1. regulates splenocyte and NK cell function in part through MEK signaling

2. Study provides evidence that Clec16a plays a key role in the survival of Purkinje cells and in the degradative function or clearance of autolysosomes.

3. CLEC16A associations in common variable immunodeficiency disorder represent the first robust evidence of non-HLA associations in this immunodeficiency condition.

4. The novel Pdx1-Clec16a-Nrdp1 pathway this study describes provides a genetic basis for the pathogenesis of mitochondrial dysfunction in multiple forms of diabetes.

5. Islets from mice with pancreas-specific deletion of Clec16a have abnormal mitochondria with reduced oxygen consumption and ATP concentration, both of which are required for normal beta cell function, Clec16a controls beta cell function and prevents diabetes by controlling mitophagy.