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Rabbit Anti-SOX17/Cy7 Conjugated antibody (bs-12205R-Cy7)
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說 明 書: 100ul  
100ul/2980.00元
大包裝/詢價
產(chǎn)品編號 bs-12205R-Cy7
英文名稱 Rabbit Anti-SOX17/Cy7 Conjugated antibody
中文名稱 Cy7標(biāo)記的轉(zhuǎn)錄因子SOX17抗體
別    名 SOX-17; SOX17_HUMAN; SRY (sex determining region Y) box 17; SRY box 17; SRY related HMG box transcription factor SOX17; Transcription factor SOX-17; Transcription factor SOX17.  
規(guī)格價格 100ul/2980元 購買        大包裝/詢價
說 明 書 100ul  
研究領(lǐng)域 發(fā)育生物學(xué)  干細(xì)胞  轉(zhuǎn)錄調(diào)節(jié)因子  表觀遺傳學(xué)  
抗體來源 Rabbit
克隆類型 Polyclonal
交叉反應(yīng) Rat,  (predicted: Human, Mouse, Chicken, Pig, Cow, )
產(chǎn)品應(yīng)用
not yet tested in other applications.
optimal dilutions/concentrations should be determined by the end user.
分 子 量 44kDa
性    狀 Lyophilized or Liquid
濃    度 1mg/ml
免 疫 原 KLH conjugated synthetic peptide derived from Human SOX17
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(chǎn)品介紹 background:
Sox genes comprise a family of genes that are related to the mammalian sex determining gene SRY. These genes similarly contain sequences that encode for the HMG-box domain, which is responsible for the sequence-specific DNA-binding activity. Sox genes encode putative transcriptional regulators implicated in the decision of cell fates during development and the control of diverse developmental processes. The highly complex group of Sox genes cluster at least 40 different loci that rapidly diverged in various animal lineages. At present, 30 Sox genes have been identified. Members of this family have been shown to be conserved during evolution and to play key roles during animal development. Some are involved in human diseases, including sex reversal.

Function:
Acts as transcription regulator that binds target promoter DNA and bends the DNA. Binds to the sequences 5'-AACAAT-'3 or 5'-AACAAAG-3'. Modulates transcriptional regulation via WNT3A. Inhibits Wnt signaling. Promotes degradation of activated CTNNB1. Plays a key role in the regulation of embryonic development. Required for normal looping of the embryonic heart tube. Required for normal development of the definitive gut endoderm. Probable transcriptional activator in the premeiotic germ cells.

Subunit:
Interacts with CTNNB1, LEF1 and TCF4 (By similarity).

Subcellular Location:
Nucleus.

Tissue Specificity:
Expressed in adult heart, lung, spleen, testis, ovary, placenta, fetal lung, and kidney. In normal gastrointestinal tract, it is preferentially expressed in esophagus, stomach and small intestine than in colon and rectum.

DISEASE:
Defects in SOX17 are the cause of vesicoureteral reflux type 3 (VUR3) [MIM:613674]. VUR3 is a disease belonging to the group of congenital anomalies of the kidney and urinary tract. It is characterized by the reflux of urine from the bladder into the ureters and sometimes into the kidneys, and is a risk factor for urinary tract infections. Primary disease results from a developmental defect of the ureterovesical junction. In combination with intrarenal reflux, the resulting inflammatory reaction may result in renal injury or scarring, also called reflux nephropathy. Extensive renal scarring impairs renal function and may predispose patients to hypertension, proteinuria, renal insufficiency and end-stage renal disease.

Similarity:
Contains 1 HMG box DNA-binding domain.
Contains 1 Sox C-terminal domain.

Database links:

Entrez Gene: 64321 Human

Entrez Gene: 20671 Mouse

Entrez Gene: 312936 Rat

Omim: 610928 Human

SwissProt: Q9H6I2 Human

SwissProt: Q61473 Mouse

Unigene: 98367 Human

Unigene: 279103 Mouse



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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