Dematin (DMTN) (NM_001114136) Human Tagged ORF Clone Lentiviral Particle

CAT#: RC225631L4V

Lenti ORF particles, DMTN (mGFP-tagged) - Human erythrocyte membrane protein band 4.9 (dematin) (EPB49), transcript variant 3, 200ul, >10^7 TU/mL

Specifications

Product Data

• Type: Human Tagged ORF Clone Lentiviral Particle
• Tag: mGFP
• Symbol: DMTN
• Synonyms: DMT; EPB49
• Mammalian Cell Selection: Puromycin
• Vector: pLenti-C-mGFP-P2A-Puro
• ACCN: NM_001114136
• ORF Size: 1215 bp
• Sequence Data:
  ORF Nucleotide Sequence

  The ORF insert of this clone is exactly the same as(RC225631).
• 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.

Reference Data

• RefSeq: NM_001114136.1, NP_001107608.1
• RefSeq Size: 2561 bp
• RefSeq ORF: 1218 bp
• Locus ID: 2039
• Cytogenetics: 8p21.3
• MW: 45.5 kDa
• Gene Summary: 'The protein encoded by this gene is an actin binding and bundling protein that plays a structural role in erythrocytes, by stabilizing and attaching the spectrin/actin cytoskeleton to the erythrocyte membrane in a phosphorylation-dependent manner. This protein contains a core domain in the N-terminus, and a headpiece domain in the C-terminus that binds F-actin. When purified from erythrocytes, this protein exists as a trimer composed of two 48 kDa polypeptides and a 52 kDa polypeptide. The different subunits arise from alternative splicing in the 3' coding region, where the headpiece domain is located. Disruption of this gene has been correlated with the autosomal dominant Marie Unna hereditary hypotrichosis disease, while loss of heterozygosity of this gene is thought to play a role in prostate cancer progression. Alternative splicing results in multiple transcript variants encoding different isoforms. [provided by RefSeq, Nov 2014]'