Akt3 (NM_011785) Mouse Tagged ORF Clone Lentiviral Particle

CAT#: MR207672L3V

Lenti ORF particles, Akt3 (Myc-DDK-tagged) - Mouse thymoma viral proto-oncogene 3 (Akt3), 200ul, >10^7 TU/mL

Specifications

Product Data

• Type: Mouse Tagged ORF Clone
• Tag: Myc-DDK
• Symbol: Akt3
• Synonyms: AI851531; D930002M15Rik; Nmf350
• Mammalian Cell Selection: Puromycin
• Vector: pLenti-C-Myc-DDK-P2A-Puro
• ACCN: NM_011785
• ORF Size: 1440 bp
• Sequence Data:
  ORF Nucleotide Sequence

  The ORF insert of this clone is exactly the same as(MR207672).
• 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_011785.2, NP_035915.2
• RefSeq Size: 4735 bp
• RefSeq ORF: 1440 bp
• Locus ID: 23797
• UniProt ID: Q9WUA6
• Cytogenetics: 1 H4
• Gene Summary: AKT3 is one of 3 closely related serine/threonine-protein kinases (AKT1, AKT2 and AKT3) called the AKT kinase, and which regulate many processes including metabolism, proliferation, cell survival, growth and angiogenesis. This is mediated through serine and/or threonine phosphorylation of a range of downstream substrates. Over 100 substrate candidates have been reported so far, but for most of them, no isoform specificity has been reported. AKT3 is the least studied AKT isoform. It plays an important role in brain development and is crucial for the viability of malignant glioma cells. AKT3 isoform may also be the key molecule in up-regulation and down-regulation of MMP13 via IL13. Required for the coordination of mitochondrial biogenesis with growth factor-induced increases in cellular energy demands. Down-regulation by RNA interference reduces the expression of the phosphorylated form of BAD, resulting in the induction of caspase-dependent apoptosis.[UniProtKB/Swiss-Prot Function]