CD62E (SELE) (NM_000450) Human Tagged ORF Clone Lentiviral Particle

SKU RC221153L1V

Lenti ORF particles, SELE (Myc-DDK tagged) - Human selectin E (SELE), 200ul, >10^7 TU/mL

Product Data

• Type: Human Tagged ORF Clone Lentiviral Particle
• Tag: Myc-DDK
• Target Symbol: CD62E
• Synonyms: CD62E; ELAM; ELAM1; ESEL; LECAM2
• Vector: pLenti-C-Myc-DDK
• Mammalian Cell Selection: None
• Sequence Data:
  ORF Nucleotide Sequence

  The ORF insert of this clone is exactly the same as(RC221153).
• ACCN: NM_000450
• ORF Size: 1830 bp
• OTI Disclaimer: The molecular sequence of this clone aligns with the gene accession number as a point of reference only. However, individual transcript sequences of the same gene can differ through naturally occurring variations (e.g. polymorphisms), each with its own valid existence. This clone is substantially in agreement with the reference, but a complete review of all prevailing variants is recommended prior to use. More info
• OTI Annotation: This clone was engineered to express the complete ORF with an expression tag. Expression varies depending on the nature of the gene.
• Shipping: Dry Ice

Reference Data

• RefSeq: NM_000450.1
• RefSeq Size: 3834 bp
• RefSeq ORF: 1833 bp
• Locus ID: 6401
• UniProt ID: P16581
• Cytogenetics: 1q24.2
• Domains: CCP, CLECT, EGF
• Protein Families: Druggable Genome, Transmembrane
• Protein Pathways: Cell adhesion molecules (CAMs)
• MW: 66.66 kDa
• Summary: The protein encoded by this gene is found in cytokine-stimulated endothelial cells and is thought to be responsible for the accumulation of blood leukocytes at sites of inflammation by mediating the adhesion of cells to the vascular lining. It exhibits structural features such as the presence of lectin- and EGF-like domains followed by short consensus repeat (SCR) domains that contain 6 conserved cysteine residues. These proteins are part of the selectin family of cell adhesion molecules. Adhesion molecules participate in the interaction between leukocytes and the endothelium and appear to be involved in the pathogenesis of atherosclerosis. [provided by RefSeq, Jul 2008]