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Claudin 16 Rabbit pAb (bs-13752R)  
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50ul/1180.00元
100ul/1980.00元
200ul/2800.00元
大包裝/詢價
產(chǎn)品編號 bs-13752R
英文名稱 Claudin 16 Rabbit pAb
中文名稱 緊密連接蛋白16抗體
別    名 Claudin 16; Claudin-16; CLD16_HUMAN; CLDN 16; Cldn16; Paracellin 1; Paracellin-1; PCLN-1; PCLN 1; PCLN1.  
Specific References  (1)     |     bs-13752R has been referenced in 1 publications.
[IF=5.717] Hwee-Yeong Ng. et al. Effect of Dapagliflozin and Magnesium Supplementation on Renal Magnesium Handling and Magnesium Homeostasis in Metabolic Syndrome. Nutrients. 2021 Nov;13(11):4088  IHC ;  Rat.  
研究領(lǐng)域 細胞生物  信號轉(zhuǎn)導  細胞粘附分子  內(nèi)皮細胞  
抗體來源 Rabbit
克隆類型 Polyclonal
交叉反應(yīng) (predicted: Human,Mouse,Rat,Rabbit,Sheep,Cow,Chicken,Dog)
產(chǎn)品應(yīng)用 IHC-P=1:100-500,IHC-F=1:100-500,IF=1:100-500,ICC/IF=1:100-500,ELISA=1:5000-10000
not yet tested in other applications.
optimal dilutions/concentrations should be determined by the end user.
理論分子量 34 kDa
檢測分子量
細胞定位 細胞膜 
性    狀 Liquid
濃    度 1mg/ml
免 疫 原 KLH conjugated synthetic peptide derived from human Claudin 16: 95-150/305 <Extracellular>
亞    型 IgG
純化方法 affinity purified by Protein A
緩 沖 液 0.01M TBS (pH7.4) with 1% BSA, 0.02% Proclin300 and 50% Glycerol.
保存條件 Shipped at 4℃. Store at -20℃ for one year. Avoid repeated freeze/thaw cycles.
注意事項 This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.
PubMed PubMed
產(chǎn)品介紹 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.

Function:
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.

Subcellular Location:
Cell junction; tight junction. Cell membrane.

Tissue Specificity:
Kidney-specific, including the thick ascending limb of Henle (TAL).

DISEASE:
Defects in CLDN16 are the cause of hypomagnesemia type 3 (HOMG3) [MIM:248250]; also known as familial hypomagnesemia with hypercalciuria and nephrocalcinosis (FHHNC). HOMG3 is a progressive renal disease characterized by primary renal magnesium wasting with hypomagnesemia, hypercalciuria and nephrocalcinosis. Recurrent urinary tract infections and kidney stones are often observed. In spite of hypercalciuria, patients do not show hypocalcemia.

Similarity:
Belongs to the claudin family.

SWISS:
Q9Y5I7

Gene ID:
10686

Database links:

Entrez Gene: 10686 Human

Entrez Gene: 114141 Mouse

Entrez Gene: 155268 Rat

Omim: 603959 Human

SwissProt: Q9Y5I7 Human

SwissProt: Q14BW2 Mouse

SwissProt: Q925N4 Mouse

SwissProt: Q91Y55 Rat

Unigene: 251391 Human

Unigene: 275205 Mouse

Unigene: 43852 Rat



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