OLFM2 (Vector pENTR223.1, Accession No. BC011361)

Length: 1365 Sequence: atgtggccgc tcacggtccc gccgccgctg ctgctgctgc tgtgctcagg cctggccgga cagactctct tccagaaccc agaagagggc tggcagctgt acacctcagc ccaggcccct gacgggaaat gcatctgcac ggccgtgatc ccagcgcaga gtacctgctc tcgagatggc aggagtcggg agctgcggca actgatggag aaggtccaga acgtctccca gtccatggag gtccttgagt tgcggacgta tcgcgacctc cagtatgtac gcggcatgga gaccctcatg cggagcctgg atgcgcggct ccgggcagct gatgggtccc tctcggccaa gagcttccag gagctgaagg acaggatgac ggaactgttg cccctgagct cggtcctgga gcagtacaag gcagacacgc ggaccattgt acgcttgcgg gaggaggtga ggaatctctc cggcagtctg gcggccattc aggaggagat gggtgcctac gggtatgagg acctgcagca acgggtgatg gccctggagg cccggctcca cgcctgcgcc cagaagctgg gctgtgggaa gctgaccggg gtcagtaacc ccatcaccgt tcgggccatg gggtcccgct tcggctcctg gatgactgac acgatggccc ccagtgcgga tagccgggtc tggtacatgg atggctatta caaaggccgc cgggtcctgg agttccgtac cctgggagac ttcatcaaag gccagaactt tatccagcac ctgctgcccc agccgtgggc gggcacgggc cacgtggtgt acaacggctc cctgttctat aacaagtacc agagcaacgt ggtggtcaaa taccacttcc gctcgcgctc tgtgctggtg cagaggagcc tcccgggcgc cggttacaac aacaccttcc cctactcctg gggcggcttc tccgacatgg acttcatggt ggacgagagc gggctctggg ctgtgtacac caccaaccag aacgcgggca acatcgtggt cagccggctg gacccgcaca ccctcgaggt catgcggtcc tgggacaccg gctaccccaa gcgcagcgct ggcgaggcct tcatgatctg cggtgtgctc tacgtgacca actcccacct ggctggggcc aaggtctact tcgcctattt taccaacacg tccagttacg agtacacgga cgtgcccttc cacaaccagt attcccacat ctcgatgctg gattacaacc cccgggagcg cgccctctat acctggaaca acggccacca ggtgctctac aatgtcaccc tgtttcacgt catcagcacc tctggggacc Protein function: 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. 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. [The UniProt Consortium]