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Sema4a encodes a member of the semaphorin family of soluble and transmembrane proteins. Additionally we are shipping Sema4a Antibodies (101) and Sema4a Proteins (13) and many more products for this protein.
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Sema4A activated the Akt (show AKT1 ELISA Kits) pathway via Plexin D1 (show PLXND1 ELISA Kits) receptor in lung fibroblasts.Lung fibroblasts show elevated levels of Sema4A expression in systemic sclerosis patients.
Data suggest that increased expression of semaphorin 4A (Sema4A) is required to promote inflammation of rheumatoid arthritis (RA).
Germline variants in SEMA4A predispose to familial colorectal cancer type X.
PACAP (show ADCYAP1 ELISA Kits) released from retinal neural cells (photoreceptors or optic nerve cells) may regulate Sema4A expression in retinal pigment epithelial cells and thereby contribute to the maintenance of retinal structure and function.
These results indicate the importance of the Sema4A protein conformation in human and mouse retina homeostasis.
Sema4A plays an inhibitory role in T helper (Th)2-type allergic diseases, such as allergic asthma, in a fraction of Sema4a-deficient transgenic mice.
mutations in SEMA4A may cause susceptibility to light exposure, oxidative stress, and ER stress, which may be involved in the progression and pathology of RP.
Dendritic cell-derived SEM4A is not only critical for T helper type (Th)1 (show TH1L ELISA Kits) cells but also for Th17 cell differentiation, and multiple sclerosis patients with high Sema4A levels exhibit Th17 cell skewing.
Mutations within the SEMA4A gene cause various retinal degnerative diseases.
SEMA4A is required for optimal activation of mTORC1 in CD8 (show CD8A ELISA Kits)+ T cells.
Treg-cell stability can be subverted in certain inflammatory sites, but is maintained by a Sema4a-Nrp1 (show NRP1 ELISA Kits) axis-- this pathway is a potential therapeutic target that could limit Treg-cell-mediated tumour-induced tolerance without inducing autoimmunity
Data indicate that both semaphorin 4A mRNA and protein were clearly detected on the earliest progenitors and were downregulated through thymic development.
A fraction of Sema4a-deficient transgenic BALB/c mice spontaneously develop skin lesions resembling atopic dermatitis (AD) in humans.
These data provide a new insight into Sema4A biology and define Sema4A as an important regulator of Th2-driven lung pathophysiology.
Sema4A activates a specialized and restricted genetic program in macrophages able to sustain angiogenesis and participates in their recruitment and activation in inflammatory injuries.
Sema4A regulates two distinct endosomal-sorting pathways that are critical for photoreceptor survival and phototransduction during the transition between daylight and darkness.
experiments using knockout mice revealed that Sema4A but not Sema7A (show SEMA7A ELISA Kits) was required for the effect produced by Th1 (show HAND1 ELISA Kits) cells on neurite outgrowth from cortical neurons.
Data indicated that Sema4A could function as a chemo-repulsive cue by activating a receptor whose signal is transmitted to Rho-kinase (show ROCK2 ELISA Kits) and induced growth cone collapse of hippocampal neurons.
This gene encodes a member of the semaphorin family of soluble and transmembrane proteins. Semaphorins are involved in numerous functions, including axon guidance, morphogenesis, carcinogenesis, and immunomodulation. The encoded protein is a single-pass type I membrane protein containing an immunoglobulin-like C2-type domain, a PSI domain and a sema domain. It inhibits axonal extension by providing local signals to specify territories inaccessible for growing axons. It is an activator of T-cell-mediated immunity and suppresses vascular endothelial growth factor (VEGF)-mediated endothelial cell migration and proliferation in vitro and angiogenesis in vivo. Mutations in this gene are associated with retinal degenerative diseases including retinitis pigmentosa type 35 (RP35) and cone-rod dystrophy type 10 (CORD10). Multiple alternatively spliced transcript variants encoding different isoforms have been identified.
, sema domain, immunoglobulin domain (Ig), transmembrane domain (TM) and short cytoplasmic domain, (semaphorin) 4A
, sema B
, semaphorin 4A