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Rabbit Anti-ARA9/XAP2/Cy7 Conjugated antibody (bs-10926R-Cy7)
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說 明 書: 100ul  
100ul/2980.00元
大包裝/詢價
產品編號 bs-10926R-Cy7
英文名稱1 Rabbit Anti-ARA9/XAP2/Cy7 Conjugated antibody
中文名稱 Cy7標記的乙型肝炎病毒X相關蛋白2抗體
別    名 AH receptor interacting protein; AH receptor-interacting protein; AIP; AIP; AIP_HUMAN; ARA 9; Aryl hydrocarbon receptor interacting protein; Aryl-hydrocarbon receptor-interacting protein; fa03h10; FKBP 16; FKBP 37; FKBP16; FKBP37; HBV X associated protein 2; HBV X associated protein; HBV X-associated protein 2; HBVX associated protein; Immunophilin homolog ARA 9; Immunophilin homolog ARA9; SMTPHN; XAP 2; XAP-2; XAP2.   
規(guī)格價格 100ul/2980元 購買        大包裝/詢價
說 明 書 100ul  
研究領域 細胞生物  神經生物學  細菌及病毒  
抗體來源 Rabbit
克隆類型 Polyclonal
交叉反應 (predicted: Human, Mouse, Rat, Dog, Cow, Horse, Rabbit, Sheep, )
產品應用
not yet tested in other applications.
optimal dilutions/concentrations should be determined by the end user.
分 子 量 38kDa
性    狀 Lyophilized or Liquid
濃    度 1mg/ml
免 疫 原 KLH conjugated synthetic peptide derived from human ARA9
亞    型 IgG
純化方法 affinity purified by Protein A
儲 存 液 0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol.
保存條件 Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. The lyophilized antibody is stable at room temperature for at least one month and for greater than a year when kept at -20°C. When reconstituted in sterile pH 7.4 0.01M PBS or diluent of antibody the antibody is stable for at least two weeks at 2-4 °C.
產品介紹 background:
The protein encoded by this gene is a receptor for aryl hydrocarbons and a ligand-activated transcription factor. The encoded protein is found in the cytoplasm as part of a multiprotein complex, but upon binding of ligand is transported to the nucleus. This protein can regulate the expression of many xenobiotic metabolizing enzymes. Also, the encoded protein can bind specifically to and inhibit the activity of hepatitis B virus. [provided by RefSeq, Sep 2008]

Function:
signaling, possibly by influencing its receptivity for ligand and/or its nuclear targeting.
Cellular negative regulator of the hepatitis B virus (HBV) X protein.May play a positive role in AHR-mediated (aromatic hydrocarbon receptor)

Subunit:
Interacts with RET in the pituitary gland; this interaction prevents the formation of the AIP-survivin complex.

Subcellular Location:
Cytoplasm.

Tissue Specificity:
Widely expressed. Higher levels seen in the heart, placenta and skeletal muscle. Not expressed in the liver.

DISEASE:
Defects in AIP are a cause of familial isolated pituitary adenoma (FIPA)
[MIM:102200]. Defects in AIP are a cause of growth hormone-secreting pituitary adenoma (GHSPA) [MIM:102200]; also known as familial isolated somatotropinomas (FIS) or isolated familial somatotropinoma (IFS) or familial somatotrophinoma or acromegaly due to pituitary adenoma.
Defects in AIP are a cause of ACTH-secreting pituitary adenoma (ASPA) [MIM:219090]; also known as pituitary Cushing disease. A pituary adenoma resulting in excessive production of adrenocorticotropic hormone. This leads to hypersecretion of cortisol by the adrenal glands and ACTH-dependent Cushing syndrome. Clinical manifestations of Cushing syndrome include facial and trunkal obesity, abdominal striae, muscular weakness, osteoporosis, arterial hypertension, diabetes.
Defects in AIP are a cause of prolactin-secreting pituitary adenoma (PSPA) [MIM:600634]; also known as prolactinoma. Prolactin-secreting pituitary adenoma is the most common type of hormonally active pituitary adenoma.

Similarity:
Contains 1 PPIase FKBP-type domain.
Contains 2 TPR repeats.

Database links:

Entrez Gene: 9049 Human

Entrez Gene: 11632 Mouse

Entrez Gene: 282827 Rat

Entrez Gene: 360190 Cow

Entrez Gene: 610467 Dog

Omim: 605555 Human

SwissProt: Q7YRC1 Cow

SwissProt: O00170 Human

SwissProt: O08915 Mouse

SwissProt: Q5FWY5 Rat

Unigene: 20864 Dog

Unigene: 412433 Human

Unigene: 10433 Mouse

Unigene: 95160 Rat



Important Note:
This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.
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