PYGL (NM_002863) Human Tagged ORF Clone Lentiviral Particle

CAT#: RC210683L3V

Lenti ORF particles, PYGL (Myc-DDK tagged) - Human phosphorylase, glycogen, liver (PYGL), transcript variant 1, 200ul, >10^7 TU/mL

Specifications

Product Data

• Type: Human Tagged ORF Clone Lentiviral Particle
• Tag: Myc-DDK
• Symbol: PYGL
• Synonyms: GSD6
• Mammalian Cell Selection: Puromycin
• Vector: pLenti-C-Myc-DDK-P2A-Puro
• ACCN: NM_002863
• ORF Size: 2541 bp
• Sequence Data:
  ORF Nucleotide Sequence

  The ORF insert of this clone is exactly the same as(RC210683).
• 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_002863.3
• RefSeq Size: 2859 bp
• RefSeq ORF: 2544 bp
• Locus ID: 5836
• UniProt ID: P06737
• Cytogenetics: 14q22.1
• Domains: phosphorylase
• Protein Families: Druggable Genome
• Protein Pathways: Insulin signaling pathway, Starch and sucrose metabolism
• MW: 97.1 kDa
• Gene Summary: This gene encodes a homodimeric protein that catalyses the cleavage of alpha-1,4-glucosidic bonds to release glucose-1-phosphate from liver glycogen stores. This protein switches from inactive phosphorylase B to active phosphorylase A by phosphorylation of serine residue 15. Activity of this enzyme is further regulated by multiple allosteric effectors and hormonal controls. Humans have three glycogen phosphorylase genes that encode distinct isozymes that are primarily expressed in liver, brain and muscle, respectively. The liver isozyme serves the glycemic demands of the body in general while the brain and muscle isozymes supply just those tissues. In glycogen storage disease type VI, also known as Hers disease, mutations in liver glycogen phosphorylase inhibit the conversion of glycogen to glucose and results in moderate hypoglycemia, mild ketosis, growth retardation and hepatomegaly. Alternative splicing results in multiple transcript variants encoding different isoforms.[provided by RefSeq, Feb 2011]