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Validated All-in-One™ qPCR Primer for SLIT2(NM_004787.3) Search again
Product ID:
HQP022584
(click here to view gene annotation page)
Species:
Human
Symbol:
Alias:
SLIL3, Slit-2
Gene Description:
slit guidance ligand 2
Target Gene Accession:
NM_004787.3(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
Gene References into function
- Analysis of alternative splicing and conserved domains in human and mouse slit genes
- SLIT2, a human homologue of the Drosophila Slit2 gene, has tumor suppressor activity and is frequently inactivated in lung and breast cancers.
- SLIT2 is an excellent candidate tumor suppressor gene for colorectal cancer.
- Our data indicate that SLIT2 is frequently inactivated by promoter region CpG island hypermethylation in gliomas and may be a good candidate for a glioma tumour suppressor gene (TSG) located at 4p15.2.
- effect of Slit (=Slit-2) on the metastatic properties of breast cancer cells
- evidence showing that Slit1 and Slit2 proteins are selective inhibitors and repellents for dorsally projecting, but not for ventrally projecting, cranial motor axons
- Slit2 inhibits vascular smooth muscle cell migration by suppressing small GTPase Rac1 activation.
- Both medulloblastoma and glioma tumors express Robo1 and Slit2, but only medulloblastoma invasion is inhibited by recombinant Slit2 protein.
- Slit-2 inhibited neurite outgrowth in stem cell cultures.
- Slit2 induces targeted migration and may play a role in brain metastasis of breast cancer cells.
- long-range Ca(2+) signaling coordinates the Slit-2-induced changes in motility at two distant parts of migrating neurons by regulating RhoA distribution
- SLIT2 mRNA decreases with vascular function decline in pulmonary fibrosis.
- Inactivation of SLIT2-ROBO1 signaling pathway may have an important role in uterine cervical carcinoma development.
- the crystal structures of the second LRR domain of human Slit2 and the minimal complex between these proteins (Slit2 D2-Robo1 Ig1).
- a chemorepulsive effect mediated by interaction of Slit2 and Robo1 participates in glioma cell guidance in the brain.
- Slit-2-overexpressing breast cancer cells exhibit tumor suppressor capabilities through the novel mechanism of beta-catenin modulation.
- Slits are negative regulators of Sdf1 and Cxcr4 in breast cancer cells.
- These results suggest that epigenetic inactivation of SLIT2 in hepatocellular carcinomas (HCC) may be important in the development and progression of HCC.
