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The findings indicate that the migration of human neural progenitor cells from the fetal subventricular zone to the olfactory bulb is partially regulated by the Slit2 (show SLIT3 Proteins)-Robo1 (show ROBO1 Proteins) axis.
Elevated SLIT2 (show SLIT3 Proteins) promoter methylation contributed to the risk of NPC (show NPC1 Proteins).
Curcumin up-regulates Slit-2 and down-regulates the expression of CXCR4 (show CXCR4 Proteins), SDF-1 (show CXCL12 Proteins), MMP2 (show MMP2 Proteins) and MMP9 (show MMP9 Proteins) in Ishikawa, Hec (show NDC80 Proteins)- 1B and primary human endometrial carcinoma cells.
The alteration of Slit2 (show SLIT3 Proteins) and Robo1 (show ROBO1 Proteins) expression in the retinas of diabetic rats and patients with proliferative diabetic retinopathy suggests a role for the Slit-Robo signal in the various stages diabetic retinopathy.
human placental multipotent mesenchymal stromal cell express Slit2 (show SLIT3 Proteins) and both Robo1 (show ROBO1 Proteins) and Robo4 (show ROBO4 Proteins) are present in human umbilical vein endothelial cells.
Slit2 (show SLIT3 Proteins)-Robo1 (show ROBO1 Proteins) signaling promoted the adhesion, invasion and migration of tongue carcinoma cells by upregulating the expression levels of MMP2 (show MMP2 Proteins) and MMP9 (show MMP9 Proteins) and, downregulating the expression of E-cadherin (show CDH1 Proteins).
findings suggest that AK3 and SLIT2 may be potential candidates involved in genetic susceptibility to colorectal cancer
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.
Both ISL1-LHX3 and ISL1-LHX4 bound to the Slit2 enhancer.
Study provides evidence that Slit2 is a novel quantitative trait gene and a positive regulator of the number and function of murine hematopoietic stem cells.
While Slit1 (show SLIT1 Proteins) and Robo2 (show ROBO2 Proteins) are only expressed in peripheral axons and their cell bodies, Slit2, Slit3 (show SLIT3 Proteins) and Robo1 (show ROBO1 Proteins) are also expressed in satellite cells of the dorsal root ganglion, Schwann cells and fibroblasts of peripheral nerves.
Transgenic over-expression of slit2 enhances disruption of blood-brain barrier and increases cell death after traumatic brain injury in mice. This suggest that over expression of slit2 plays a detrimental role in the pathophysiology of mild TBI.
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
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
Combining Slit2 with VEGFs adjusts VEGFR2 (show KDR Proteins)-mediated angiogenic effects into a more physiological direction
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
, slit homolog 2 (Drosophila)