CLDN19 Antibody

1. permeability barriers and affected cell morphology, proliferation, migration, AKT signaling, and gene expression. When claudins are exogenously expressed, ARPE-19 more closely model native RPE. PMID: 27593915
2. CLDN19 genetic mutation is responsible for familial magnesium deficiency with hypercalciuria and nephrocalcinosis. PMID: 25410674
3. analysis of a novel mutation c.241C>T in exon 2 of CLDN19 in a Chinese patient PMID: 25555744
4. Claudin-19, the most abundant claudin in myelin, exhibited no binding to ZO2 protein. PMID: 25712527
5. patients with CLDN19 mutations have a high risk of progression to chronic renal disease PMID: 23301036
6. Case Reports: novel CLDN19 mutation in familial hypomagnesemia with hypercalciuria and nephrocalcinosis. PMID: 23538362
7. The risk of end-stage renal disease in patients with CLDN19 mutations was two times the risk of patients with CLDN16 mutations. Ocular abnormalities were observed only in patients with CLDN19 mutations. PMID: 22422540
8. In a patient with consanguineous parents, history of disturbed organization and development of the retina, a diagnosis of Familial hypomagnesemia with hypercalciuria and nephrocalcinosis caused by claudin-19 mutation should be considered. PMID: 22734304
9. Ocular manifestations and exercise intolerance mimicking mild to moderate periodic paralysis are two symptoms that may occur in patients with familial hypomagnesemia with hypercalciuria and nephrocalcinosis and may indicate CLDN19 mutations. PMID: 21030577
10. The identification of CLDN19 mutations in patients with chronic renal failure and severe visual impairment supports the fundamental role of claudin-19 for normal renal tubular function and undisturbed organization and development of the retina. PMID: 17033971

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HGNC: 2040

OMIM: 248190

KEGG: hsa:149461

STRING: 9606.ENSP00000296387

UniGene: Hs.496270