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抗人 PAR6 抗体对
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抗人 PAR6 抗体对

01AB02754

Par-6 family cell polarity regulator alpha (PAR6α), encoded by PARD6A, is a cytoplasmic scaffold protein that is a core component of the evolutionarily conserved Par3–Par6–atypical PKC (aPKC) polarity complex. It contains an N‑terminal PB1 domain that heterodimerizes with aPKC, a semi‑CRIB motif binding active Cdc42/Rac1, and a C‑terminal PDZ domain that associates with Par3 and other polarity proteins, thereby linking Cdc42 to Par3–aPKC and organizing tight junctions and apical–basal polarity in epithelial cells. Through this complex, PAR6α regulates epithelial morphogenesis, directional migration, axon specification, and coupling of polarity to apoptosis via an aPKC–GSK3β pathway. PAR6 overexpression induces epidermal growth factor–independent proliferation of mammary epithelial cells by activating MEK/ERK signaling and is frequently upregulated in precancerous breast lesions and estrogen receptor–positive breast cancers, where it promotes hyperplastic acinar growth and contributes to tumor initiation and progression.

Human
规格起售价
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技术参数

靶点基因名
PARD6A
基因别名
PAR6A
蛋白别名
par-6 family cell polarity regulator alpha; PAR6
UniProt
Q9NPB6
物种
Human

产品详情

靶点名称
PAR6
蛋白名称
par-6 family cell polarity regulator alpha
蛋白别名
Partitioning defective 6 homolog alpha; PAR-6; PAR-6 alpha; PAR-6A; PAR6C; Tax interaction protein 40; TIP-40
靶点基因名
PARD6A
基因别名
PAR6A
UniProt
Q9NPB6
来源物种
Homo sapiens (Human)
物种反应性
Human

背景介绍

Par-6 family cell polarity regulator alpha (PAR6α), encoded by PARD6A, is a cytoplasmic scaffold protein that is a core component of the evolutionarily conserved Par3–Par6–atypical PKC (aPKC) polarity complex. It contains an N‑terminal PB1 domain that heterodimerizes with aPKC, a semi‑CRIB motif binding active Cdc42/Rac1, and a C‑terminal PDZ domain that associates with Par3 and other polarity proteins, thereby linking Cdc42 to Par3–aPKC and organizing tight junctions and apical–basal polarity in epithelial cells. Through this complex, PAR6α regulates epithelial morphogenesis, directional migration, axon specification, and coupling of polarity to apoptosis via an aPKC–GSK3β pathway. PAR6 overexpression induces epidermal growth factor–independent proliferation of mammary epithelial cells by activating MEK/ERK signaling and is frequently upregulated in precancerous breast lesions and estrogen receptor–positive breast cancers, where it promotes hyperplastic acinar growth and contributes to tumor initiation and progression.