Kir6.2 (KCNJ11) (NM_000525) Human Tagged ORF Clone Lentiviral Particle

SKU RC209103L3V

Lenti ORF particles, KCNJ11 (Myc-DDK tagged) - Human potassium inwardly-rectifying channel, subfamily J, member 11 (KCNJ11), transcript variant 1, 200ul, >10^7 TU/mL

Product Data

• Type: Human Tagged ORF Clone Lentiviral Particle
• Tag: Myc-DDK
• Target Symbol: Kir6.2
• Synonyms: BIR; HHF2; IKATP; KIR6.2; MODY13; PHHI; PNDM2; TNDM3
• Vector: pLenti-C-Myc-DDK-P2A-Puro
• Mammalian Cell Selection: Puromycin
• Sequence Data:
  ORF Nucleotide Sequence

  The ORF insert of this clone is exactly the same as(RC209103).
• ACCN: NM_000525
• ORF Size: 1170 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_000525.3
• RefSeq Size: 3418 bp
• RefSeq ORF: 1173 bp
• Locus ID: 3767
• Cytogenetics: 11p15.1
• Protein Families: Druggable Genome, Ion Channels: Potassium, Transmembrane
• Protein Pathways: Type II diabetes mellitus
• MW: 43.5 kDa
• Summary: Potassium channels are present in most mammalian cells, where they participate in a wide range of physiologic responses. The protein encoded by this gene is an integral membrane protein and inward-rectifier type potassium channel. The encoded protein, which has a greater tendency to allow potassium to flow into a cell rather than out of a cell, is controlled by G-proteins and is found associated with the sulfonylurea receptor SUR. Mutations in this gene are a cause of familial persistent hyperinsulinemic hypoglycemia of infancy (PHHI), an autosomal recessive disorder characterized by unregulated insulin secretion. Defects in this gene may also contribute to autosomal dominant non-insulin-dependent diabetes mellitus type II (NIDDM), transient neonatal diabetes mellitus type 3 (TNDM3), and permanent neonatal diabetes mellitus (PNDM). Multiple alternatively spliced transcript variants that encode different protein isoforms have been described for this gene. [provided by RefSeq, Oct 2009]