抗Human SLIT3 抗体:
抗Mouse (Murine) SLIT3 抗体:
抗Rat (Rattus) SLIT3 抗体:
Polyclonal SLIT3 Primary Antibody for ELISA, WB - ABIN539481
Holmes, Negus, Burridge, Raman, Algar, Yamada, Little: Distinct but overlapping expression patterns of two vertebrate slit homologs implies functional roles in CNS development and organogenesis. in Mechanisms of development 1999
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Human Polyclonal SLIT3 Primary Antibody for WB - ABIN4892104
Ng, Chow, Man, Yau, Wan, Iyer, Kwan, Poon, Pang, Law: Suppression of Slit3 induces tumor proliferation and chemoresistance in hepatocellular carcinoma through activation of GSK3β/β-catenin pathway. in BMC cancer 2019
Slit3 (and slit-2) coordinate neuron axonal pathfinding within the embryonic axon tracts along with Robo2 and Dcc-Netrin1.
Data show that Hedgehog signaling is required for commissure formation, glial bridge formation, and the restricted expression of the guidance molecules slit1a, slit2, slit3 and sema3d.
SLIT3 and SPARCL1 can be regulated by DNA methylation and down-regulated in lung adenocarcinoma
High genetic risk scores of SLIT3, PLEKHA5 and PPP2R2C variants increase susceptibility to increased insulin resistance by 50% and its risk may be exacerbated by consuming more than 10 cups coffee/week or 220 mg caffeine/day.
This study suggests that Slit3 acts as a tumor suppressor in hepatocellular carcinoma by repressing the tumor growth and thus tumor progression
Overexpression of Slit3 induces its tumor suppressive effects in Breast cancer.
Results show that silencing of Slit3 promoted proliferation, migration and invasion of A549 cells and induced epithelial-mesenchymal transition suggesting that Slit3 functions as a tumor suppressor in lung carcinoma.
Estrogen-dependent expression of SLIT3 may play a key role in regulating nerve-vessel interactions within the complex microenvironment of endometriosis lesions.
SLIT3 is increased with labour, and both amnion and myometrial studies describe a pro-inflammatory effect of SLIT3 in these tissues.
High SLIT3 expression is associated with high-grade gliomas.
SLIT3-ROBO4 activation promotes vascular network formation in human engineered tissue and angiogenesis in vivo.
results implicate the involvement of miR-218-2 and its host gene SLIT3 in thyroid cancer cell invasion, migration, and proliferation
Slit3 treatment increased the in vivo homing efficiency of CD34 HSPCs to the BM in NOD/SCID mice, whereas Slit3-exposed HSPC migration in vitro was inhibited. Results support a role for Slit3 in human HSPC migration in vitro and homing in vivo.
three major members (Slit2/3 and Robo1) of Slit/Robo family are widely expressed in the human normal and malignant ovarian tissues; but Slit/Robo signaling may not play an important role in regulating human ovarian cancer cell proliferation and migration
SLIT3 duplication on 5q35.1 predisposes to major depressive disorder
The chemorepellent Slit3 promotes monocyte migration.
Slit3 inhibits Robo3-induced invasion of synovial fibroblasts in rheumatoid arthritis.
Analysis of alternative splicing and conserved domains in human and mouse slit genes
Many variants in SLIT3 tend to associate with schizophrenia susceptibility in the Chinese Han population.
data suggest that Slit proteins play a key role in guiding dorsally projecting cranial motoneurons and in facilitating their neural tube exit
In fetal and embryonic stem cell cultures Slit-3 inhibited neurite outgrowth.
Slits are negative regulators of Sdf1 and Cxcr4 in breast cancer cells.
these results indicate that SLIT3 plays an osteoprotective role by synchronously stimulating bone formation and inhibiting bone resorption, making it a potential therapeutic target for metabolic bone diseases.
these indicate that SLIT3/ROBO2 promotes chondrocyte maturation via the inhibition of beta-catenin signaling.
A small truncated recombinant SLIT3 protein increased bone mass in an osteopenic mouse model.
While Slit1 and Robo2 are only expressed in peripheral axons and their cell bodies, Slit2, Slit3 and Robo1 are also expressed in satellite cells of the dorsal root ganglion, Schwann cells and fibroblasts of peripheral nerves.
Cardiac defects in mutants for Robo or Slit range from membranous ventricular septum defects to bicuspid aortic valves.
These observations from mutant Slit and Robo mice give great support for Slit/Robo role in neural crest cell migration during Enteric Nervous System development.
Heparan sulfate-deficient mouse endothelial cells was used to determine the co-reception function of heparan sulfate in Slit3-induced endothelial cell migration.
FREM1-deficient mice faithfully recapitulate many of the phenotypes seen in individuals with FREM1 deficiency and that variations in GATA4 and SLIT3 expression modulate some FREM1-related phenotypes in mice.
Report role of Slit3 in development of the caval veins and pericardium.
Robo-2-mediated targeting of P2 axons along the dorsoventral axis of the OB is controlled by Slit-3 expression
Study identify that the homeobox gene Nkx2-5 is required for early ventral restriction of Slit3 and that the T-box transcription factor Tbx2 mediates repression of Slit3 in nonchamber myocardium.
During blood vessel development, Slit3 gene expression (and that of Slit2) are linked to posttranscriptional regulation of Robo receptors.
role in regulating development of the diaphragm
Data suggest that the Slit family of axon guidance molecules (Slit 1-3) and their Robo 1 and 2 receptors contribute to the topographic targeting of basal vomeronasal axons.
Experiments with triple mutant mice demonstrate a key role for Slit3 signaling in vertebrate midline commissural axon guidance.
Slit-3 and Robo-2 expression is restricted to specific, complementary subsets of mesenchyme
functions to promote angiogenesis in coordinating organogenesis during embryonic development
The protein encoded by this gene is secreted, likely interacting with roundabout homolog receptors to effect cell migration. Two transcript variants encoding different isoforms have been found for this gene.
slit homolog 3
, slit homolog 3 protein
, slit homolog 3 (Drosophila)
, slit homolog 3 protein-like
, multiple EGF-like domains protein 5
, multiple epidermal growth factor-like domains protein 5
, multiple epidermal growth factor-like domains 5