GJB2 (NM_004004) Human Tagged ORF Clone Lentiviral Particle

CAT#: RC202092L1V

Lenti ORF particles, GJB2 (Myc-DDK tagged) - Human gap junction protein, beta 2, 26kDa (GJB2), 200ul, >10^7 TU/mL

Specifications

Product Data

• Type: Human Tagged ORF Clone Lentiviral Particle
• Tag: Myc-DDK
• Symbol: GJB2
• Synonyms: BAPS; CX26; DFNA3; DFNA3A; DFNB1; DFNB1A; HID; KID; NSRD1; PPK
• Mammalian Cell Selection: None
• Vector: pLenti-C-Myc-DDK
• ACCN: NM_004004
• ORF Size: 678 bp
• Sequence Data:
  ORF Nucleotide Sequence

  The ORF insert of this clone is exactly the same as(RC202092).
• 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_004004.3
• RefSeq Size: 2347 bp
• RefSeq ORF: 681 bp
• Locus ID: 2706
• UniProt ID: P29033
• Cytogenetics: 13q12.11
• Protein Families: Druggable Genome, Ion Channels: Other, Transmembrane
• MW: 26.2 kDa
• Gene Summary: This gene encodes a member of the gap junction protein family. The gap junctions were first characterized by electron microscopy as regionally specialized structures on plasma membranes of contacting adherent cells. These structures were shown to consist of cell-to-cell channels that facilitate the transfer of ions and small molecules between cells. The gap junction proteins, also known as connexins, purified from fractions of enriched gap junctions from different tissues differ. According to sequence similarities at the nucleotide and amino acid levels, the gap junction proteins are divided into two categories, alpha and beta. Mutations in this gene are responsible for as much as 50% of pre-lingual, recessive deafness. [provided by RefSeq, Oct 2008]