• Target：
• Claudin-19

• Fields：
• >>Cell adhesion molecules;>>Tight junction;>>Leukocyte transendothelial migration;>>Pathogenic Escherichia coli infection;>>Hepatitis C

• Gene Name：
• CLDN19

• Protein Name：
• Claudin-19

• Human Gene Id：
• 149461

• Human Swiss Prot No：
• Q8N6F1

• Mouse Swiss Prot No：
• Q9ET38

• Rat Gene Id：
• 298487

• Rat Swiss Prot No：
• Q5QT56

• Immunogen：
• The antiserum was produced against synthesized peptide derived from human CLDN19. AA range:81-130

• Specificity：
• Claudin-19 Polyclonal Antibody detects endogenous levels of Claudin-19 protein.

• Formulation：
• Liquid in PBS containing 50% glycerol, 0.5% BSA and 0.02% sodium azide.

• Source：
• Polyclonal, Rabbit,IgG

• Dilution：
• WB 1:500 - 1:2000. ELISA: 1:10000. Not yet tested in other applications.

• Purification：
• The antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen.

• Concentration：
• 1 mg/ml

• Storage Stability：
• -15°C to -25°C/1 year(Do not lower than -25°C)

• Other Name：
• CLDN19;Claudin-19

• Observed Band(KD)：
• 23kD

• Background：
• The product of this gene belongs to the claudin family. It plays a major role in tight junction-specific obliteration of the intercellular space, through calcium-independent cell-adhesion activity. Defects in this gene are the cause of hypomagnesemia renal with ocular involvement (HOMGO). HOMGO is a progressive renal disease characterized by primary renal magnesium wasting with hypomagnesemia, hypercalciuria and nephrocalcinosis associated with severe ocular abnormalities such as bilateral chorioretinal scars, macular colobomata, significant myopia and nystagmus. Alternatively spliced transcript variants encoding distinct isoforms have been identified for this gene. [provided by RefSeq, Jun 2010],

• Function：
• disease:Defects in CLDN19 are the cause of hypomagnesemia renal with ocular involvement (HOMGO) [MIM:248190]. HOMGO is a progressive renal disease characterized by primary renal magnesium wasting with hypomagnesemia, hypercalciuria and nephrocalcinosis associated with severe ocular abnormalities such as bilateral chorioretinal scars, macular colobomata, significant myopia and nystagmus. The renal phenotype is virtually undistinguishable from that of patients with HOMG3 with proven CLDN16 mutations.,function:Plays a major role in tight junction-specific obliteration of the intercellular space, through calcium-independent cell-adhesion activity.,similarity:Belongs to the claudin family.,

• Subcellular Location：
• Cell junction, tight junction. Cell membrane; Multi-pass membrane protein.

• Expression：
• Kidney,Lung,Spleen,

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