OLFM2 (NM_058164) Human Tagged ORF Clone Lentiviral Particle

SKU RC203786L1V

Lenti ORF particles, OLFM2 (Myc-DDK tagged) - Human olfactomedin 2 (OLFM2), 200ul, >10^7 TU/mL

Product Data

• Type: Human Tagged ORF Clone Lentiviral Particle
• Tag: Myc-DDK
• Target Symbol: OLFM2
• Synonyms: NOE2; NOELIN2; NOELIN2_V1; OlfC
• 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(RC203786).
• ACCN: NM_058164
• ORF Size: 1362 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_058164.1
• RefSeq Size: 1899 bp
• RefSeq ORF: 1365 bp
• Locus ID: 93145
• UniProt ID: O95897
• Cytogenetics: 19p13.2
• Domains: OLF
• Protein Families: Druggable Genome, Secreted Protein
• MW: 51.4 kDa
• Summary: Involved in transforming growth factor beta (TGF-beta)-induced smooth muscle differentiation. TGF-beta induces expression and translocation of OLFM2 to the nucleus where it binds to SRF, causing its dissociation from the transcriptional repressor HEY2/HERP1 and facilitating binding of SRF to target genes (PubMed:25298399). Plays a role in AMPAR complex organization (By similarity). Is a regulator of vascular smooth-muscle cell (SMC) phenotypic switching, that acts by promoting RUNX2 and inhibiting MYOCD binding to SRF. SMC phenotypic switching is the process through which vascular SMCs undergo transition between a quiescent contractile phenotype and a proliferative synthetic phenotype in response to pathological stimuli. SMC phenotypic plasticity is essential for vascular development and remodeling (By similarity).[UniProtKB/Swiss-Prot Function]