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Rabbit Anti-phospho-HNF4 (Ser313)/AP Conjugated antibody (bs-4001R-AP)
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說 明 書: 100ul  
100ul/2980.00元
大包裝/詢價(jià)
產(chǎn)品編號(hào) bs-4001R-AP
英文名稱 Rabbit Anti-phospho-HNF4 (Ser313)/AP Conjugated antibody
中文名稱 堿性磷酸酶(AP)標(biāo)記的磷酸化肝細(xì)胞核因子4α抗體
別    名 HNF4 (phospho S313); p-HNF4 (phospho S313); Hepatic nuclear factor 4 alpha; Hepatocyte nuclear factor 4 alpha; Hepatocyte nuclear factor 4; HNF 4 alpha; HNF 4; HNF4; HNF4A; HNF4a7; HNF4a8; HNF4a9; Hnf4alpha; MODY 1; MODY; MODY1; NR2A1; NR2A21; Nuclear receptor subfamily 2 group A member 1; TCF 14; TCF; TCF14; Tcf4; Transcription factor 14, hepatic nuclear factor; Transcription factor 14; Transcription factor HNF 4; Transcription factor HNF4.  
規(guī)格價(jià)格 100ul/2980元 購(gòu)買        大包裝/詢價(jià)
說 明 書 100ul  
產(chǎn)品類型 磷酸化抗體 乙?;贵w 
研究領(lǐng)域 腫瘤  免疫學(xué)  染色質(zhì)和核信號(hào)  信號(hào)轉(zhuǎn)導(dǎo)  轉(zhuǎn)錄調(diào)節(jié)因子  激酶和磷酸酶  
抗體來源 Rabbit
克隆類型 Polyclonal
交叉反應(yīng) (predicted: Human, Mouse, Rat, Chicken, Pig, Cow, Horse, Rabbit, Guinea Pig, )
產(chǎn)品應(yīng)用 WB=1:50-200 
not yet tested in other applications.
optimal dilutions/concentrations should be determined by the end user.
分 子 量 52kDa
性    狀 Lyophilized or Liquid
濃    度 1mg/ml
免 疫 原 KLH conjugated Synthesised phosphopeptide derived from human HNF4 alpha around the phosphorylation site of Ser313
亞    型 IgG
純化方法 affinity purified by Protein A
儲(chǔ) 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(chǎn)品介紹 background:
The protein encoded by the HNF4 gene is a nuclear transcription factor which binds DNA as a homodimer. The encoded protein controls the expression of several genes, including hepatocyte nuclear factor 1 alpha, a transcription factor which regulates the expression of several hepatic genes. This gene may play a role in development of the liver, kidney, and intestines. Mutations in this gene have been associated with monogenic autosomal dominant non insulin dependent diabetes mellitus type I. At least three different transcript variants encoding three different isoforms have been found for this gene.

Function:
Transcriptionally controlled transcription factor. Binds to DNA sites required for the transcription of alpha 1-antitrypsin, apolipoprotein CIII, transthyretin genes and HNF1-alpha. May be essential for development of the liver, kidney and intestine.

Subunit:
Homodimerization is required for HNF4-alpha to bind to its recognition site.

Subcellular Location:
Nucleus.

Post-translational modifications:
Phosphorylated on tyrosine residue(s); phosphorylation is important for its DNA-binding activity. Phosphorylation may directly or indirectly play a regulatory role in the subnuclear distribution. Phosphorylation at Ser-313 by AMPK reduces the ability to form homodimers and bind DNA.
Acetylation at Lys-458 lowers transcriptional activation by about two-fold.

DISEASE:
Defects in HNF4A are the cause of maturity-onset diabetes of the young type 1 (MODY1) [MIM:125850]; also symbolized MODY-1. MODY is a form of diabetes that is characterized by an autosomal dominant mode of inheritance, onset in childhood or early adulthood (usually before 25 years of age), a primary defect in insulin secretion and frequent insulin-independence at the beginning of the disease.

Similarity:
Belongs to the nuclear hormone receptor family. NR2 subfamily.
Contains 1 nuclear receptor DNA-binding domain.

Database links:

Entrez Gene: 3172 Human

Entrez Gene: 15378 Mouse

Entrez Gene: 25735 Rat

Omim: 600281 Human

SwissProt: P41235 Human

SwissProt: P49698 Mouse

SwissProt: P22449 Rat

Unigene: 116462 Human

Unigene: 202383 Mouse

Unigene: 12238 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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