CLDN19 antibody - C-terminal region (ARP33619_P050)
- Known as:
- CLDN19 (anti-) - C-terminal region (ARP33619_P050)
- Catalog number:
- arp33619_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- CLDN19 antibody - C-terminal region (ARP33619_P050)
Related genes to: CLDN19 antibody - C-terminal region (ARP33619_P050)
- Gene:
- CLDN19 NIH gene
- Name:
- claudin 19
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 1p34.2
- Locus Type:
- gene with protein product
- Date approved:
- 2000-03-15
- Date modifiied:
- 2015-08-24
Related products to: CLDN19 antibody - C-terminal region (ARP33619_P050)
Related articles to: CLDN19 antibody - C-terminal region (ARP33619_P050)
- Claudin-16 ( and claudin-19 ( are essential tight junction proteins in the kidney that are critical for magnesium homeostasis. Mutations in and cause Familial Hypomagnesemia with Hypercalciuria and Nephrocalcinosis (FHHNC), a rare autosomal recessive tubular disorder. The disorder can progressively lead to severe complications, including end-stage renal disease. Affected individuals often present with polyuria, polydipsia, nephrolithiasis, hematuria, muscular tetany, seizures, and failure to thrive. Notably, mutations have also been associated with ocular abnormalities. We describe three patients with FHHNC and ocular involvement harboring a novel homozygous variant of uncertain significance (VUS) in the gene (). Our findings contribute to the expanding genetic landscape of this rare disorder and highlight the importance of early diagnosis and multidisciplinary management. - Source: PubMed
Publication date: 2026/08/24
Alhothali WajdaHijazi ShahdAlharbi EbtehalAl Fakeeh KhalidAl Qahtani Abdullah TAlmannai MohammedAl Tuwaijri AbeerEyaid WafaaAlfreihi Shatha - Magnesium is an essential mineral involved in numerous physiological and neurobiological processes. However, the biological effects of distinct Mg forms remain insufficiently characterized. This study compared the systemic and neurobiological effects of a multi-form Mg supplement (Magnesium Breakthrough™, Mg BT™, , Reno, NV, USA) with commonly used single-form Mg compounds in a rat model. Sixty-day-old male Wistar rats were assigned to a control group or to groups receiving Mg BT™ or individual Mg compounds (oxide, citrate or glycinate). Treatments were administered by gastric gavage for 30 days at 50 mg/kg/day of elemental Mg. A comprehensive panel of endpoints was evaluated, including Mg distribution in biological fluids and tissues, metabolic markers, glucose tolerance, synaptic protein expression (synaptophysin, PSD95, phospho-PSD95, drebrin), cortical gene expression (NR2B, BDNF), behavioral outcomes, and liver and kidney histology. Magnesium from the multi-form supplement increased serum Mg without affecting glucose homeostasis and modulated proteins involved in synaptic plasticity, accompanied by mild anxiolytic-like effects without changes in locomotion. No adverse histological alterations were observed, while preserved renal CLDN-19 expression indicated maintained tubular integrity. These findings suggest that supplementation with the multi-form Mg BT™ supplement influences multiple evaluated biological domains, including systemic, behavioral and molecular parameters, with effects comparable to those observed with individual magnesium compounds under the experimental conditions applied. - Source: PubMed
Publication date: 2026/07/24
Dizdar MuamerObučić MoniaCrnčević NeiraDinić SvetlanaUskoković AleksandraJovanović Jelena ArambašićBorković-Mitić SlavicaMladenović AleksandraMilanović DesankaPraćer SmiljaNestorović NatašaManojlović-Stojanoski MilicaMihailović MirjanaPavlović Slađan - FAT atypical cadherin 2 (FAT2), a member of the protocadherin superfamily involved in cell adhesion and polarity, remains incompletely characterized in breast cancer. This study aimed to elucidate the expression pattern, clinical significance, and functional mechanisms of FAT2 in breast cancer. - Source: PubMed
Publication date: 2026/04/13
Xie GangyinLu DengweiLi ZiweiXu Tao - Familial hypomagnesaemia with hypercalciuria and nephrocalcinosis (FHHNC) is a rare autosomal recessive tubulopathy caused by mutations in the CLDN16 or CLDN19 genes, patients usually develop hypomagnesemia, hypercalciuria, nephrocalcinosis and renal failure early in life, and those with CLDN19 gene mutations have ocular findings in addition. Five children from four non-consanguineous Chinese Han families presenting with nephrocalcinosis and renal insufficiency were enrolled in our study. Metabolic profiling and radiology examinations were performed, in addition to whole exome sequencing (WES) used for detection of the causative variant. Clinical manifestations included polydipsia, polyuria, sterile leukocyturia or urinary tract infections. Meanwhile, hypomagnesemia was observed in the entire cohort on laboratory analyses. One patient presented with hemorrhagic ovarian cyst and proteinuria, and the renal biopsy revealed tubulointerstitial injury accompanied by glomerular sclerosis. Whole-exome sequencing identified four patients with compound heterozygosity in the CLDN16 gene, [c.217+5G>A]; [ c.218_382del], [c.130C>T]; [c.158delA] and [c.436C>T]; [c.158delA], and one patient with compound heterozygosity in the CLDN19 gene for the c.223G > S (p.G75S) variant and a novel frameshift pathogenic variant c.2;20delG (p.D74Tfs*10), which has not been previously reported in PubMed or ClinVar. Importantly, an unusual phenotype of hemorrhagic ovarian cyst was observed in one patient carrying CLDN16 mutations (c.217+5 (IVS2)G>A and c.218_382del). For the first time, we identified a novel CLDN19 pathogenic variant and documented hemorrhagic ovarian cyst in a patient with CLDN16 mutations. This study represents the largest multi-family analysis of FHHNC in a Chinese population cohort. Integrated clinical and genetic analyses of our patients might help to offer preliminary insights that contribute to refining the phenotypic and genotypic spectrum of this rare renal disorder. - Source: PubMed
Publication date: 2026/03/27
Wang ChunDing JuanjuanYang HuihuiHuang LinWang Xiaowen - The blood-retinal barrier (BRB) maintains neurovascular homeostasis by regulating solute and ion exchange between the retina and circulation. This selectivity depends on tight junctions (TJs), with claudin (Cldn) proteins forming the core structure that defines paracellular permeability. Distinct Cldn isoforms show cell-specific expression, with Cldn-5 predominating in the endothelial cells of the inner BRB and Cldn-19 is the signature Cldn in the retinal pigment epithelium forming the outer BRB. Disruption of these isoforms contributes to vascular leakage, inflammation, and neuronal loss across various ocular diseases. Cldn function in vascular homeostasis is multifaceted; barrier dysfunction does not always result from Cldn loss, as excessive expression or mislocalization, particularly of Cldn-5, can also impair BRB integrity. Cldns act as dynamic signaling hubs that respond to metabolic, oxidative, and mechanical stress and are regulated through VEGF, Wnt/β-catenin, and RhoA/ROCK pathways. This review summarizes current understanding of Cldn biology in retinal vascular regulation and highlights emerging therapeutic strategies aimed at stabilizing Cldn expression and junctional localization. Small molecules and blocking antibodies that enhance localization or prevent degradation are redefining barrier repair. Key questions remain regarding isoform specificity, inter-barrier communication, and systemic safety. Integrative omics and spatial imaging may reveal disease-specific Cldn signatures and guide molecular restoration of BRB integrity. - Source: PubMed
Publication date: 2026/02/27
Selim Mohamed SNarayanan S PriyaSomanath Payaningal R