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These data supports a model whereby Wnt signaling through Frizzled-3a attenuates expression of Slit2 in the rostral midline of the forebrain.
In embryonic axon tracts, Robo2 (show ROBO2 Proteins) responds to signals from slit2 and slit3 (show SLIT3 Proteins).
Data show that Hedgehog (show SHH Proteins) signaling is required for commissure formation, glial bridge formation, and the restricted expression of the guidance molecules slit1a, slit2, slit3 (show SLIT3 Proteins) and sema3d (show SEMA3D Proteins).
Slit acts via Robo2 (show ROBO2 Proteins) in dendrites as a branching/growth factor but not in guidance, while Robo2 (show ROBO2 Proteins) and Robo3 (show ROBO3 Proteins) function in concert in axons to mediate axonal interactions and respond to Slits as guidance factors
Low Slit2 expression is associated with glioma.
Results indicate the importance of SLIT2 (show SLIT3 Proteins)-ROBO1 (show ROBO1 Proteins)-CDC42 (show CDC42 Proteins) signaling pathway in predicting tumor progression.
We postulate that Robo1 (show ROBO1 Proteins) promotes tumor invasion partly by the upregulation of MMP2 (show MMP2 Proteins) after activation of PI3K (show PIK3CA Proteins)/Akt (show AKT1 Proteins) signaling pathway. Notably, Slit2 (show SLIT3 Proteins) knockdown caused the upregulation of Robo1 (show ROBO1 Proteins) expression both at the mRNA and protein levels. Thus, the stimulatory effects of Slit2 (show SLIT3 Proteins) knockdown on tumor progression can be ascribed, at least in part, to the upregulation of Robo1 (show ROBO1 Proteins) and its positive role in tumor progression.
expression of the evolutionarily conserved slit2 (show SLIT3 Proteins) Gene Promoter Requires Sp1 (show PSG1 Proteins)
Study shows that Slit2 (show SLIT3 Proteins) mRNA and protein levels were significantly reduced in papillary thyroid cancer (PTC (show F9 Proteins)) specimens and implicates Slit2 (show SLIT3 Proteins) functions as a negative regulator in the development and progression of PTC (show F9 Proteins).
Overexpression of Slit2 induces its tumor suppressive effects in Breast cancer.
Significantly increased serum Slit2 (show SLIT3 Proteins) levels and hepatic expression of Slit2 (show SLIT3 Proteins) and Robo1 (show ROBO1 Proteins) were observed in patients with liver fibrosis.
our findings indicated that Slit2 (show SLIT3 Proteins)/Robo1 (show ROBO1 Proteins) axis possibly be regarded as a significant clinical parameter for predicting brain metastasis in breast cancer patients.
These results suggest that Slit2/Robo1 binding exerts an effect on cell migration, which is negatively regulated by Robo4, and Robo1 may function by interacting with CdGAP in HUVECs.
VEGFR2 (show KDR Proteins) activation was not affected by Slit2 (show SLIT3 Proteins), but eNOS (show NOS3 Proteins) phosphorylation was diminished
Slit2 induces a robust activation of PKA signaling, which is required for its prothermogenic activity.
Robo1-Slit2 interaction required for pathfinding mechanism essential to establish the functionally important habenulo-interpeduncular connection.
Together, these observations suggest that Slit2 serves as a factor utilized by muscle Ctnnb1 (show CTNNB1 Proteins) to direct presynaptic differentiation.
Slit2 acts as a repellant cue to mediate axon guidance in the formation of the anterior commissure.
Slit2/Robo1 (show ROBO1 Proteins) signaling promotes intestinal tumorigenesis through Src (show SRC Proteins)-mediated activation of the Wnt (show WNT2 Proteins)/beta-catenin (show CTNNB1 Proteins) pathway.
the two genes neuropeptide Y (Npy (show NPY Proteins)) and Slit homolog 2 (Drosophila) (Slit2) gradually increase during aging, and upon suppression of these two genes
Data shows that modulation of angiostatic factor Slit2 by EphA2 receptor regulates endothelial responses to VEGF-mediated angiogenesis and tumor neovascularization.
administration of Slit2 to atherosclerosis-prone LDL receptor (show LDLR Proteins)-deficient mice inhibited monocyte recruitment to nascent atherosclerotic lesions.
Results provide novel evidence that low expression of SLIT2 correlates with poor prognosis and promotes metastasis in ESCC, which may be regulated by the Cdc42 (show CDC42 Proteins)-mediated pathways.
Slit2 may promote angiogenesis by upregulating Robo1 and activating the VEGFR2-ERK1/2 pathway.
acts as a ligand for glypican-1, a heparan sulfate proteoglycan\; may play a role in neurogenesis and midline development
slit homolog 2 protein
, downregulated during adipocyte differentiation-1
, neurogenic extracellular slit protein