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Sema4a encodes a member of the semaphorin family of soluble and transmembrane proteins. Zusätzlich bieten wir Ihnen Sema4a Antikörper (106) und Sema4a Proteine (15) und viele weitere Produktgruppen zu diesem Protein an.
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Human oligodendrocytes undergo apoptosis when exposed to Sema4A and take up H-ferritin for meeting iron requirements and that these functions are mediated via the Tim-1 receptor. H-ferritin can block Sema4A-mediated cytotoxicity. Sema4A is detectable in the CSF of multiple sclerosis patients and HIV-seropositive persons and can induce oligodendrocyte cell death.
Advanced peri-implantitis lesions showed higher levels of gene expression for Sem3A and Sem4D and lower levels of Sem4A in comparison to tissues obtained from a healthy dental implant.
Here we show three families with retinal degeneration in which unaffected family members are either homozygous or heterozygous for the variant. The p.R713Q variant in SEMA4A is insufficient to cause either autosomal recessive or autosomal dominant retinitis pigmentosa and is unlikely to be pathogenic.
ILT-4 is a receptor for hSEMA4A)on activated CD4(+) T cells. hSEMA4A is highly expressed in human asthmatic lung tissue.
Suggest a role for Plexin-B1 as a ligand and Sema4A as a receptor and characterize a reverse signaling pathway downstream of Sema4A regulating cell migration via Scrib.
SEMA 4A confers doxorubicin resistance on hepatocellular carcinoma by inducing epithelialemesenchymal transition.
In this review, we summarized the current findings on neuroimmune Sema4A and Sema4D molecules in chronic inflammation underlying many diseases and discussed their positive or negative impacts on the implicated molecular and cellular processes
Sema4A activated the Akt pathway via Plexin D1 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 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 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+ T cells.
Treg-cell stability can be subverted in certain inflammatory sites, but is maintained by a Sema4a-Nrp1 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 was required for the effect produced by Th1 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 and induced growth cone collapse of hippocampal neurons.
These results indicated that Sema4A is critically involved in experimental autoimmune myocarditis by regulating differentiation of T-cells.
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