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人 Integrin beta-2 抗体对
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人 Integrin beta-2 抗体对

01AB01744

Integrin subunit beta 2 (Integrin beta-2) is a transmembrane glycoprotein that serves as the common β chain for the leukocyte-specific integrins αLβ2 (LFA-1), αMβ2 (Mac-1), αXβ2, and αDβ2. These heterodimers are essential adhesion receptors that bind to ligands such as ICAM-1 and fibrinogen, mediating leukocyte adhesion, extravasation, and complement-driven phagocytosis during immune responses. The activity of β2 integrins is tightly regulated by conformational changes that couple the cytoplasmic tail to the actin cytoskeleton. Germline loss-of-function mutations in the ITGB2 gene cause leukocyte adhesion deficiency type I (LAD-I). This clinical condition is characterized by recurrent severe bacterial infections, impaired wound healing, and a lack of neutrophil extravasation, often requiring hematopoietic stem cell transplantation for survival.

Human
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技术参数

靶点基因名
ITGB2
基因别名
CD18; MFI7
蛋白别名
integrin subunit beta 2; Integrin beta-2
UniProt
P05107
物种
Human

产品详情

靶点名称
Integrin beta-2
蛋白名称
integrin subunit beta 2
蛋白别名
Integrin beta-2; Cell surface adhesion glycoproteins LFA-1/CR3/p150; 95 subunit beta; Complement receptor C3 subunit beta; CD antigen CD18
靶点基因名
ITGB2
基因别名
CD18; MFI7
UniProt
P05107
来源物种
Homo sapiens (Human)
物种反应性
Human

背景介绍

Integrin subunit beta 2 (Integrin beta-2) is a transmembrane glycoprotein that serves as the common β chain for the leukocyte-specific integrins αLβ2 (LFA-1), αMβ2 (Mac-1), αXβ2, and αDβ2. These heterodimers are essential adhesion receptors that bind to ligands such as ICAM-1 and fibrinogen, mediating leukocyte adhesion, extravasation, and complement-driven phagocytosis during immune responses. The activity of β2 integrins is tightly regulated by conformational changes that couple the cytoplasmic tail to the actin cytoskeleton. Germline loss-of-function mutations in the ITGB2 gene cause leukocyte adhesion deficiency type I (LAD-I). This clinical condition is characterized by recurrent severe bacterial infections, impaired wound healing, and a lack of neutrophil extravasation, often requiring hematopoietic stem cell transplantation for survival.