Use your antibodies-online credentials, if available.
No Products on your Comparison List.
Your basket is empty.
Find out more
Show all synonyms
Select your origin of interest
The novel CAPN5 mutation (p.R289W) is responsible for the present autosomal dominant neovascular inflammatory vitreoretinopathy (ADNIV) family. The mutant CAPN5 stimulated secretion and cleavage of SLIT2 fragments that may act as a bystander to regulate abnormal RPE cell proliferation for ADNIV.
an interaction between the BMP2-Gremlin and SLIT2 pathways in human kidney cells
SLIT2/ROBO1 signalling may regulate trophoblast differentiation and invasion causing restricting beta human chorionic gonadotrophin (beta-hCG) production, shallow trophoblast invasion and inhibiting placental angiogenesis in missed and threatened miscarriage during the first trimester.
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-Robo1 axis.
Elevated SLIT2 promoter methylation contributed to the risk of NPC.
Curcumin up-regulates Slit-2 and down-regulates the expression of CXCR4, SDF-1, MMP2 and MMP9 in Ishikawa, Hec- 1B and primary human endometrial carcinoma cells.
The alteration of Slit2 and Robo1 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 and both Robo1 and Robo4 are present in human umbilical vein endothelial cells.
Slit2-Robo1 signaling promoted the adhesion, invasion and migration of tongue carcinoma cells by upregulating the expression levels of MMP2 and MMP9 and, downregulating the expression of E-cadherin.
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-ROBO1-CDC42 signaling pathway in predicting tumor progression.
We postulate that Robo1 promotes tumor invasion partly by the upregulation of MMP2 after activation of PI3K/Akt signaling pathway. Notably, Slit2 knockdown caused the upregulation of Robo1 expression both at the mRNA and protein levels. Thus, the stimulatory effects of Slit2 knockdown on tumor progression can be ascribed, at least in part, to the upregulation of Robo1 and its positive role in tumor progression.
expression of the evolutionarily conserved slit2 Gene Promoter Requires Sp1
Study shows that Slit2 mRNA and protein levels were significantly reduced in papillary thyroid cancer (PTC) specimens and implicates Slit2 functions as a negative regulator in the development and progression of PTC.
Overexpression of Slit2 induces its tumor suppressive effects in Breast cancer.
Significantly increased serum Slit2 levels and hepatic expression of Slit2 and Robo1 were observed in patients with liver fibrosis.
temporary up-regulation in remodeling vessel and down-regulation in remodeled vessel of polygonal-shape extravillous trophoblast cells occurred in tubal pregnancies
our findings indicated that Slit2/Robo1 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.
Trio induces RhoA activation downstream of Slit2, and support a functional role in ensuring the proper positioning of both guidepost cells and a major axonal tract.
High Slit-2 expression is associated with hepatic fibrosis.
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.
Contralateral migration of oculomotor neurons is regulated by Slit/Robo signaling. Results demonstrate that a migratory subset of motor neurons respond to floor plate-derived Slit repulsion to properly control the timing of contralateral migration.
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.
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.
overexpression promoted vascular remodeling by increasing the diameter of the maternal blood sinusoids and fetal capillaries
Together, these observations suggest that Slit2 serves as a factor utilized by muscle Ctnnb1 to direct presynaptic differentiation.
Slit2 acts as a repellant cue to mediate axon guidance in the formation of the anterior commissure.
Slit2/Robo1 signaling promotes intestinal tumorigenesis through Src-mediated activation of the Wnt/beta-catenin pathway.
the two genes neuropeptide Y (Npy) and Slit homolog 2 (Drosophila) (Slit2) gradually increase during aging, and upon suppression of these two genes
Cardiac defects in mutants for Robo or Slit range from membranous ventricular septum defects to bicuspid aortic valves.
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-deficient mice inhibited monocyte recruitment to nascent atherosclerotic lesions.
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.
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-mediated pathways.
Slit2 may promote angiogenesis by upregulating Robo1 and activating the VEGFR2-ERK1/2 pathway.
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 responds to signals from slit2 and slit3.
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.
Slit acts via Robo2 in dendrites as a branching/growth factor but not in guidance, while Robo2 and Robo3 function in concert in axons to mediate axonal interactions and respond to Slits as guidance factors
Combining Slit2 with VEGFs adjusts VEGFR2-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)