Semaphorin 7A, GPI membrane anchor (John Milton Hagen blood group) (SEMA7A) also known as CD108 (C luster of D ifferentiation 108), is a human gene. [5] SEMA7A is a membrane-bound semaphorin that associates with cell surfaces via a glycosylphosphatidylinositol (GPI) linkage.

2024年12月25日 · SEMA7A (Semaphorin 7A (JohnMiltonHagen Blood Group)) is a Protein Coding gene. Diseases associated with SEMA7A include Cholestasis, Progressive Familial Intrahepatic, 11 and Blood Group, John Milton Hagen System. Among its related pathways are Nervous system development and Semaphorin interactions.

2023年1月30日 · Semaphorin7a (SEMA7A), a membrane-anchored member of the semaphorin protein family, could be involved in a diverse range of immune responses via its receptor integrin β1.

2017年1月21日 · Semaphorin 7A (Sema7A) is expressed by several different classes of lymphoid and myeloid cells and is a potent immunomodulator. We examined the role of Sema7A in modulating cellular immune responses and to provide experimental data validating the therapeutic potential of Sema7A in rheumatoid arthritis (RA).

2024年5月29日 · Recent work has shown that semaphorin 7A (Sema7A) holds significant impact on platelet function, yet its role on neutrophil function within the lung is not well understood. This study aimed to identify the role of Sema7A during pulmonary inflammation and sepsis.

Granular cytoplasmic and membranous expression in several tissues, most abundant in testis and gastrointestinal tract. Main subcellular location based on data generated in the subcellular section of the Human Protein Atlas.

94 results presented herein show that SEMA7A mRNA expression is highest in patients with ER+ 95 BC and that SEMA7A induces pleiotropic tumor-promotional effects in ER+BC cells. We also 96 describe a novel relationship between hormone signaling and expression of SEMA7A in BC.

2021年1月4日 · Here we report that semaphorin 7A (SEMA7A) confers significantly decreased patient survival rates in ER + breast cancer. SEMA7A was hormonally regulated in ER + breast cancer, but its expression did not uniformly decrease with antiestrogen treatments.

2016年1月1日 · We demonstrate that Sema7A deficiency results in impaired chemokine CCL21-driven DC migration in vivo. Impaired formation of actin-based protrusions, resulting in slower three-dimensional migration, was identified as the mechanism underlying the DC migration defect.

Genetic variations in SEMA7A define the John Milton Hagen blood group system (JMH) [MIM:614745]. Three different JMH phenotypes have been identified based on the presence or absence of the high-frequency JMH antigen: JMH-weak, JMH-negative, and JMH-variant.