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WAS (基因名), Wiskott-Aldrich syndrome protein (蛋白名), wasp_human.
产品名称:

Human WAS/ Wiskott-Aldrich syndrome protein Recombinant Protein
Wiskott-Aldrich综合症蛋白质

货号:

R1917h

商标:
EIAab®
监管等级:
别名:

WASp, IMD2

序列号:
P42768
来源:
E.coli
种属:
Human
标签:
His
纯度:
>90% by SDS-PAGE
浓度:
Reconstitution Dependent
形态:
Liquid
内毒素水平:
Please contact protein@eiaab.com The technician for more information.
应用:
存储缓冲液:
50mM NaH2PO4, 500mM NaCl Buffer with 500mM Imidazole, 10%glycerol(PH8.0)
存储:
Store at -20°C. (Avoid repeated freezing and thawing.)
研究领域:
-
Human WAS Protein
规格 & 价格: cart
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Human WAS Protein
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产品说明书
说明书: 下载说明书
MSDS: MSDS
在线询价


R&D 技术数据
更多信息,请参阅手册,或联系我们的技术支持: tech@eiaab.com.
基因位点
Cytogenetic band: Xp11.23 by HGNC Xp11.23 by Entrez Gene Xp11.23 by Ensembl
WAS Gene in genomic location: bands according to Ensembl, locations according to GeneLoc (and/or Entrez Gene and/or Ensembl if different)
基因位点
通用注释


亚单元:
Interacts with NCK1 (via SH3 domains) (By similarity). Interacts with CDC42, RAC, NCK, HCK, FYN, SRC kinase FGR, BTK, ABL1, PSTPIP1, WIP, and to the p85 subunit of PLC-gamma. Binds the Arp2/3 complex. Interacts (via C-terminus) with ALDOA. Interacts with E.coli effector protein EspF(U).


功能:
Effector protein for Rho-type GTPases. Regulates actin filament reorganization via its interaction with the Arp2/3 complex. Important for efficient actin polymerization. Possible regulator of lymphocyte and platelet function. Mediates actin filament reorganization and the formation of actin pedestals upon infection by pathogenic bacteria.


亚细胞位置:
Cytoplasm Cytoskeleton


该产品尚未在任何出版物中被引用。

[1].
"Chemical inhibition of N-WASP by stabilization of a native autoinhibited conformation."

[2].
"Phosphorylation of the WASP-VCA domain increases its affinity for the Arp2/3 complex and enhances actin polymerization by WASP."

[3].
"Phosphorylation of tyrosine 291 enhances the ability of WASp to stimulate actin polymerization and filopodium formation. Wiskott-Aldrich Syndrome protein."

[4].
"Constitutively activating mutation in WASP causes X-linked severe congenital neutropenia."

[5].
"The identification and characterization of two promoters and the complete genomic sequence for the Wiskott-Aldrich syndrome gene."

[6].
"Defective actin polymerization in EBV-transformed B-cell lines from patients with the Wiskott-Aldrich syndrome."

[7].
"Variable expression of WASP in B cell lines of Wiskott-Aldrich syndrome patients."

[8].
"Wiskott-Aldrich syndrome protein, a novel effector for the GTPase CDC42Hs, is implicated in actin polymerization."

[9].
"X-linked thrombocytopenia and Wiskott-Aldrich syndrome are allelic diseases with mutations in the WASP gene."

[10].
"Identification of WASP mutations in patients with Wiskott-Aldrich syndrome and isolated thrombocytopenia reveals allelic heterogeneity at the WAS locus."
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