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Validated All-in-One™ qPCR Primer for NECTIN1(NM_002855.4) Search again
Product ID:
HQP015956
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
CD111, CLPED1, ED4, HIgR, HV1S, HVEC, OFC7, PRR, PRR1, PVRL1, PVRR, PVRR1, SK-12, nectin-1
Gene Description:
nectin cell adhesion molecule 1
Target Gene Accession:
NM_002855.4(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.
Gene References into function
- evidence that nectin-1 confined to adherens junctions in epithelial cells is not very accessible to virus, whereas dissociation of cell junctions releases nectin-1 to serve more efficiently as an entry receptor
- Regions of nectin-1 protein important for herpesvirus entry activity and homotypic nectin-nectin interactions are overlapping but not identical.
- association of HVEM and nectin-1 with lipid rafts during herpes simplex virus entry
- both nectin 1 and HVEM receptors play a role during HSV infection in vivo and both are highly efficient even at low levels of expression
- Nectin-1-Delta2 exhibited a severely reduced ability to mediate HSV entry and accumulated in the endoplasmic reticulum but retained the ability to interact with its HSV ligand, gD.
- trans-interacting nectin inhibits non-trans-interacting E-cadherin endocytosis through afadin, Rap1, and p120ctn and further accumulates non-trans-interacting E-cadherin to the nectin-based cell-cell adhesion sites for the formation of adherens junctions
- mutations at codons 185 and 323, especially the W185X mutation, do not participate in the formation of cleft lip and palate within the Taiwanese population examined
- Mutations within the PVRL1 gene represent risk factors for non-syndromic cleft lip with or without cleft palate.
- Access to nectin-1 contributes to preferential apical infection of human epithelial cells by herpes simplex virus.
- the role of PVRL1 in the sporadic forms of orofacial clefting in multiple populations was studied.
- nectin-1 may be used as a marker to predict the sensitivity of a tumor to herpes oncolytic therapy
- These data suggest that the determinants of gD-mediated internalization of nectin-1 may direct HSV to an endocytic pathway during entry.
- Novel non-synonymous PVRL1 mutation of the substitution of valine by methionine a position 395 in a conserved sequence suggests a possible etiologic role of PVRL1 in non-syndromic CL/P across different populations.
- Western blot analyses demonstrated that accumulation of host nectin-1 is decreased by 85 % at 48 hours post-infection (h.p.i.) in Chlamydia trachomatis serovar E-infected HeLa cells.
- Antibodies against nectin-1, but not HVEM, were able to block HSV-1 infection.Anti-nectin-1 antibodies and F-actin depolymerizers were also successful in blocking the cytoskeletal changes that occur upon HSV-1 entry into cells