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Rabbit Anti-Activin Receptor Type IIB/BF350 Conjugated antibody (bs-12417R-BF350)
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說(shuō) 明 書(shū): 100ul  
100ul/2980.00元
大包裝/詢(xún)價(jià)
產(chǎn)品編號(hào) bs-12417R-BF350
英文名稱(chēng)1 Rabbit Anti-Activin Receptor Type IIB/BF350 Conjugated antibody
中文名稱(chēng) BF350標(biāo)記的激活素受體2B抗體
別    名 Activin Receptor Type IIB; ACTR-IIB; Activin A receptor type IIB; Activin receptor type 2B; Activin receptor type IIB; Activin receptor type-2B; ActR IIB; ACTR-IIB; ActRIIB; ACVR 2B; ACVR2B; AVR2B_HUMAN; HTX4; MGC116908.  
規(guī)格價(jià)格 100ul/2980元 購(gòu)買(mǎi)        大包裝/詢(xún)價(jià)
說(shuō) 明 書(shū) 100ul  
研究領(lǐng)域 細(xì)胞生物  信號(hào)轉(zhuǎn)導(dǎo)  干細(xì)胞  生長(zhǎng)因子和激素  激酶和磷酸酶  細(xì)胞表面分子  
抗體來(lái)源 Rabbit
克隆類(lèi)型 Polyclonal
交叉反應(yīng) (predicted: Human, Mouse, Rat, Dog, Pig, Cow, Sheep, )
產(chǎn)品應(yīng)用 ICC=1:50-200 IF=1:50-200 
not yet tested in other applications.
optimal dilutions/concentrations should be determined by the end user.
分 子 量 56kDa
性    狀 Lyophilized or Liquid
濃    度 1mg/ml
免 疫 原 KLH conjugated synthetic peptide derived from human ACVR2B/ACTR-IIB
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:
Members of the transforming growth factor b superfamily bind to a pair of transmembrane proteins, known as receptor types I and II, which contain serine/threonine kinases and associate to form a signaling complex (1). Activin has been shown to bind a heteromeric noncovalent complex, which consists of a type I receptor, ACTR-IA (also designated ACVRI and ALK-2) or ACTR-IB (also designated ALK-4 and SKR2), and a type II receptor, ACTR-IIA (also designated ACVR2A) or ACTR-IIB (also designated ACVR2B) (1-6). Both receptor types are highly expressed in brain (5). The activin receptor family members are thought to mediate distinct effects on gene expression, cell differentiation, and morpho- genesis in a dose dependent fashion (5,6).

Function:
On ligand binding, forms a receptor complex consisting of two type II and two type I transmembrane serine/threonine kinases. Type II receptors phosphorylate and activate type I receptors which autophosphorylate, then bind and activate SMAD transcriptional regulators. Receptor for activin A, activin B and inhibin A.

Subunit:
Forms an activin receptor complex with activin type II receptors such as ACVR1B. Interacts with VPS39.

Subcellular Location:
Cell membrane; Single-pass type I membrane protein.

Post-translational modifications:
Phosphorylated. Constitutive phosphorylation is in part catalyzed by its own kinase activity.

DISEASE:
Defects in ACVR2B are the cause of visceral heterotaxy autosomal type 4 (HTX4) [MIM:613751]. A form of visceral heterotaxy, a complex disorder due to disruption of the normal left-right asymmetry of the thoracoabdominal organs. It results in an abnormal arrangement of visceral organs, and a wide variety of congenital defects. Clinical features of visceral heterotaxy type 4 include dextrocardia, right aortic arch and a right-sided spleen, anomalies of the inferior and the superior vena cava, atrial ventricular canal defect with dextro-transposed great arteries, pulmonary stenosis, polysplenia and midline liver.

Similarity:
Belongs to the protein kinase superfamily. TKL Ser/Thr protein kinase family.
TGFB receptor subfamily.
Contains 1 protein kinase domain.

Database links:

Entrez Gene: 93 Human

Entrez Gene: 11481 Mouse

Entrez Gene: 25366 Rat

Omim: 602730 Human

SwissProt: Q13705 Human

SwissProt: P27040 Mouse

SwissProt: P38445 Rat

Unigene: 174273 Human

Unigene: 390239 Mouse

Unigene: 24240 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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