Claudin 16 Antibody Blocking Peptide(bs-13752P)-500ug

Claudin 16 Antibody Blocking P

eptide(bs-13752P)-500ug
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  • bs-13752P
  • 2025年10月16日
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      500ug

    产品编号bs-13752P
    英文名称Claudin 16 Antibody Blocking Peptide
    中文名称紧密连接蛋白16封闭多肽
    英文别名Claudin 16; Claudin-16; CLD16_HUMAN; CLDN 16; Cldn16; Paracellin 1; Paracellin-1; PCLN-1; PCLN 1; PCLN1.
    纯化方法HPLC
    研究领域

    Signal Transduction > Cytoskeleton / ECM > Cell Adhesion > Tight Junctions

    亚细胞定位Cell junction; tight junction. Cell membrane.
    组织特异性Kidney-specific, including the thick ascending limb of Henle (TAL).
    相似性Belongs to the claudin family.
    功能Plays a major role in tight junction-specific obliteration of the intercellular space, through calcium-independent cell-adhesion activity. Involved in paracellular magnesium reabsorption. Required for a selective paracellular conductance. May form, alone or in partnership with other constituents, an intercellular pore permitting paracellular passage of magnesium and calcium ions down their electrochemical gradients. Alternatively, it could be a sensor of magnesium concentration that could alter paracellular permeability mediated by other factors.
    保存条件Shipped at 4℃. Stored at -20℃ for one year. Avoid repeated freeze/thaw cycles.
    注意事项This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.
    背景资料Tight junctions mediate the regulation of the paracellular pathway between epithelial and endothelial cells. They form close connections to eliminate the extracellular space and regulate the flow of solutes between cells. The human gene PCLN-1 (paracellin-1) is related to the claudin family of integral membrane proteins, which localize to tight junctions. PCLN-1 contains four transmembrane domains and intracellular amino and carboxy termini, characteristic of the other claudin family members, and is detected only at the tight junctions of kidney tissue. PCLN-1 forms an intercellular pore and controls the resorption of magnesium and calcium in the thick ascending limb of Henle (TAL). Mutations in PCLN-1 cause renal magnesium wasting, which may contribute to a rare autosomal recessive disease, renal hypomagnesemia with hypercalciuria and nephrocalcinosis.

     

     

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