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信号通路Wnt5a抗体1948
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中文名称信号通路Wnt5a抗体
别 名wingless-related MMTV integration site 5A; hWNT 5A; hWNT5A; Protein Wnt 5a; Protein Wnt5a; Wingless type MMTV integration site family member 5A; Wnt-5a; WNT 5A protein precursor; WNT5A protein precursor; WNT5A_HUMAN.
研究领域 肿瘤 细胞生物 信号转导
抗体来源 Rabbit
克隆类型 Polyclonal
交叉反应 Human, Mouse, Rat, (predicted: Pig, Cow, Rabbit, )
产品应用 WB=1:500-2000 ELISA=1:500-1000 IHC-P=1:100-500 IHC-F=1:100-500 Flow-Cyt=1ug/Test IF=1:100-500 (石蜡切片需做抗原修复)
not yet tested in other applications.
optimal dilutions/concentrations should be determined by the end user.
分 子 量 35kDa
细胞定位 细胞外基质 分泌型蛋白
性 状 Liquid
浓 度 1mg/ml
免 疫 原 KLH conjugated synthetic peptide derived from human WNT5A:301-381/381
亚 型 IgG
纯化方法 affinity purified by Protein A
储 存 液 0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol.
保存条件 Shipped at 4℃. Store at -20 °C for one year. Avoid repeated freeze/thaw cycles.
PubMed PubMed
产品介绍 The WNT gene family consists of structurally related genes which encode secreted signaling proteins. These proteins have been implicated in oncogenesis and in several developmental processes, including regulation of cell fate and patterning during embryogenesis. This gene encodes a member of the WNT family that signals through both the canonical and non-canonical WNT pathways. This protein is a ligand for the seven transmembrane receptor frizzled-5 and the tyrosine kinase orphan receptor 2. This protein plays an essential role in regulating developmental pathways during embryogenesis. This protein may also play a role in oncogenesis. Mutations in this gene are the cause of autosomal dominant Robinow syndrome. Alternate splicing results in multiple transcript variants. [provided by RefSeq, Jan 2012].
Function:
Ligand for members of the frizzled family of seven transmembrane receptors. Can activate or inhibit canonical Wnt signaling, depending on receptor context. In the presence of FZD4, activates beta-catenin signaling. In the presence of ROR2, inhibits the canonical Wnt pathway by promoting beta-catenin degradation through a GSK3-independent pathway which involves down-regulation of beta-catenin-induced reporter gene expression. Suppression of the canonical pathway allows chondrogenesis to occur and inhibits tumor formation. Stimulates cell migration. Decreases proliferation, migration, invasiveness and clonogenicity of carcinoma cells and may act as a tumor suppressor. Mediates motility of melanoma cells. Required during embryogenesis for extension of the primary anterior-posterior axis and for outgrowth of limbs and the genital tubercle. Inhibits type II collagen expression in chondrocytes.
Subunit:
Interacts with PORCN. Interacts with WLS.
Subcellular Location:
Secreted, extracellular space, extracellular matrix.
Tissue Specificity:
Expression is increased in differentiated thyroid carcinomas compared to normal thyroid tissue and anaplastic thyroid tumors where expression is low or undetectable. Expression is found in thyrocytes but not in stromal cells (at protein level).
Post-translational modifications:
Palmitoylation is necessary for stimulation of cell migration, inhibition of the beta-catenin pathway and receptor binding.
Glycosylation is necessary for secretion but not for activity.
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