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Mouse (Murine) SEMA3A Protein expressed in Human Cells - ABIN2008081
Chadborn, Ahmed, Holt, Prinjha, Dunn, Jones, Eickholt: PTEN couples Sema3A signalling to growth cone collapse. in Journal of cell science 2006
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Semaphorin 3A is overexpressed in urothelial cancer patients, as evidenced both in its presence in urine and in bladder tissue.
the inhibitory effect of Sema3C on microcapillary formation by human umbilical vein endothelial cells could be abrogated upon mutation at the Sema3C basic domain within putative furin cleavage site 742RNRR745, indicating that this site was essential for the Sema3 biological activity.
Results provide evidence that SEMA3A is highly expressed in glioblastoma (GBM) compared to non-neoplastic brain tissues and SEMA3A signaling axis promotes GBM growth and invasion.
these findings shows that miR-362 promotes lung cancer metastasis through downregulation of Sema3A
These findings indicate a regulatory mechanism and a proapoptotic function of aberrant Sema3A signaling in Osteoarthritis (OA) chondrocytes, and suggest that targeting Sema3A signaling might interfere OA pathogenesis.
increased concentrations of urinary SEMA-3A and urinary Netrin-1 are found in urine from children with severe hydronephrosis and that their concentrations are related to the degree of obstruction.
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.
clinical samples from apical periodontitis patients were obtained to analyse the expression of Sema3A/Nrp1. These results indicated that the bone destruction level expanded from days 7 to 35
study demonstrates that Sema3E/plexinD1 inhibits proliferation and migration of vascular smooth muscle cells via inactivation of Rap1-AKT signalling pathways
Results showed a preferential association of NRP1 with SEMA3A, suggesting that SEMA3A can partially reverse the effects caused by the VEGFA preventing its binding with the NRP1 receptor.
Our observation of a second case supports the notion that bi-allelic mutations in SEMA3A cause an autosomal recessive type of syndromic short stature.
the upregulation of SEMA3A in hepatocellular carcinoma (HCC)cells promoted tumor growth and progression in an HCC mouse model. These results indicate that SEMA3A enhances CapG, galectin-3, enolase 2 and EpCAM expression to promote HCC progression and is a potential therapeutic target for HCC.
Sema3A as a novel regulator of airway smooth cell proliferation by suppressing Rac1, GSK-3beta and STAT3 signaling mediated by Nrp1.
provide an easy and reproducible method to analyze growth cone sensitivity to the prototypic guidance molecule family class 3 semaphorin
Measuring electrical impedance allows real-time monitoring of changes in endothelial cell morphology and adhesion induced by SEMA3E via plexin D1
describe a method where in vitro cultures of growth cones are incubated with these ligands in the presence or absence of Sema3A, followed by stripping of remaining ligand on cell-surface and analysis by immunofluorescence techniques
Semaphorin 3A increased tumor-infiltrating macrophages (TAM) infiltration and promoted hepatocellular carcinoma (HCC) progression. Semaphorin 3A expression alone, or combined with the number of TAMs, is a new prognostic factor and potential target for the treatment of HCC.
Significant genetic risk for Hirschsprung disease (HSCR) was imparted by rs2435357 and rs2506030 at RET and by rs12707682 at SEMA3 in a Chinese population. No evidence was found of a genetic association between HSCR and either of the NRG1 SNPs rs7835688 and rs16879552, at either allele or genotype level.
rs139438618 at the semaphorin 3A locus was significantly associated with Alcohol Dependence and Major Depression comorbidity in African Americans. There was no significant association identified in European American participants.
Serum level of Sema3A taken from diagnosed celiac without gluten-free diet was higher significantly than healthy controls.
Study shows that despite demonstrating that they could achieve highly efficient gene deletion, disruption of Sema3A-Npn1 signaling did not affect the normal maintenance of the neuromuscular junction or disrupt motor axon reinnervation after a denervating injury.
GAS5 could ameliorate cardiomyocyte apoptosis induced by Myocardial infarction via down-regulating sema3a.
SEMA3A expression is increased in the endothelin receptor-B null mouse model of Hirschsprung disease, suggesting that SEMA3A may interfere with enteric neural crest cell migration, resulting in an absence of enteric neurons.
Our results demonstrated that overexpression of Sema3A in oral cancer cells drastically suppressed tumor growth by inhibiting angiogenesis.
a novel role for Sema3A-neuropilin 1 signalling in progenitor cell dynamics and in the generation of interneurons in the ventral telencephalon
Sema3A reduces cardiac inflammation and improves cardiac function after myocardial infarction by promoting the resolution of inflammation.
The findings highlight an active role for satellite cell-secreted Sema3A ligand as a key "commitment factor" for the slow-fiber population during muscle regeneration.
This approach can be used to study responses to repulsive guidance factors such as semaphorin 3A. Here I describe the procedures used to prepare cultured neurons for rotary-shadow EM, allowing detailed comparisons of cytoskeletal structure
Sema3a-Nrp2 signaling along an unrecognized pancreatic developmental axis constitutes a chemoattractant system essential for generating the hallmark morphogenetic properties of pancreatic islets.
These data suggest that both Nrp1 and Sema3a are expressed in the cochlea during time points when spiral ganglion cell begin to innervate the organ of Corti.
We show that PTP-3, a LAR homolog in Caenorhabditis elegans, participates in Sema2A-regulated axon guidance. PTPdelta, a member of vertebrate LAR class PTPs, is involved in Sema3A-regulated cortical dendritic growth. In Sema3A signaling, PTPdelta activates Fyn and Src kinases by dephosphorylating their C-terminal Tyr residues.
Investigated the effects of BotoxA-induced paralysis on the sprouting capacity of neuromuscular junctions (NMJs) in the K108N-SEMA3A mutant, and observed no change in the differential neuronal plasticity found at NMJs on fast-fatigable or slow muscle fibers due to the presence of the SEMA3A mutant protein.
The aim was to elucidate whether ectopic muscles are a result of misguidance of myoblast precursors due to the loss of Sema3A-Npn-1 signaling.
These findings suggest that by interacting with PlexA4, TrkA plays a crucial role in redirecting local Sema3A signaling to retrograde axonal transport, thereby regulating dendritic GluA2 localization and patterning.
Findings indicate that Rho and ROCK knockout may improve the behavior of mice and prevent MPTP-induced dopaminergic neurons damage by regulating Sema3A, PlexinA and NRP-1 in a mouse model of Parkinson's disease.
Sema3A signaling exerts its oncogenic effect by promoting an mTORC1-mediated metabolic shift from oxidative phosphorylation to aerobic glycolysis.
Semaphorin 3A (Sema3A) is a protein secreted during the development of the nervous system that acts as a cue for axon induction .
this paper shows that Nav1.7, by coupling with CRMP1, mediates the axonal retrograde signaling of Sema3A in axonal guidance
Sema3a1 is a guidance factor for neural growth cones and has a role in the development of the vascular system
Sema3a1 plays an essential role in guiding the caudal primary (CaP) motor axon that pioneers the initial region of the motor pathway.
This gene is a member of the semaphorin family and encodes a protein with an Ig-like C2-type (immunoglobulin-like) domain, a PSI domain and a Sema domain. This secreted protein can function as either a chemorepulsive agent, inhibiting axonal outgrowth, or as a chemoattractive agent, stimulating the growth of apical dendrites. In both cases, the protein is vital for normal neuronal pattern development. Increased expression of this protein is associated with schizophrenia and is seen in a variety of human tumor cell lines. Also, aberrant release of this protein is associated with the progression of Alzheimer's disease.
, semaphorin D
, semaphorin III
, semaphorin L
, sema domain, immunoglobulin domain (Ig), short basic domain, secreted, (semaphorin) 3A
, sema D
, sema III
, Semaphorin 3a
, sema domain, immunoglobulin domain (Ig), short basic domain, sec
, semaphorin 3A
, sema Z1A
, semaphorin 1a