Prkag3 (NM_153744) Mouse Tagged ORF Clone Lentiviral Particle

CAT#: MR225341L3V

Lenti ORF particles, Prkag3 (Myc-DDK-tagged) - Mouse protein kinase, AMP-activated, gamma 3 non-catatlytic subunit (Prkag3), 200ul, >10^7 TU/mL

Specifications

Product Data

• Type: Mouse Tagged ORF Clone
• Tag: Myc-DDK
• Symbol: Prkag3
• Synonyms: Amkg3; Ampkg3; AMPKg3L; AMPKg3S
• Mammalian Cell Selection: Puromycin
• Vector: pLenti-C-Myc-DDK-P2A-Puro
• ACCN: NM_153744
• ORF Size: 1467 bp
• Sequence Data:
  ORF Nucleotide Sequence

  The ORF insert of this clone is exactly the same as(MR225341).
• 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_153744.3, NP_714966.1
• RefSeq Size: 2835 bp
• RefSeq ORF: 1470 bp
• Locus ID: 241113
• UniProt ID: Q8BGM7
• Cytogenetics: 1 C4
• Gene Summary: AMP/ATP-binding subunit of AMP-activated protein kinase (AMPK), an energy sensor protein kinase that plays a key role in regulating cellular energy metabolism. In response to reduction of intracellular ATP levels, AMPK activates energy-producing pathways and inhibits energy-consuming processes: inhibits protein, carbohydrate and lipid biosynthesis, as well as cell growth and proliferation. AMPK acts via direct phosphorylation of metabolic enzymes, and by longer-term effects via phosphorylation of transcription regulators. Also acts as a regulator of cellular polarity by remodeling the actin cytoskeleton; probably by indirectly activating myosin. Gamma non-catalytic subunit mediates binding to AMP, ADP and ATP, leading to activate or inhibit AMPK: AMP-binding results in allosteric activation of alpha catalytic subunit (PRKAA1 or PRKAA2) both by inducing phosphorylation and preventing dephosphorylation of catalytic subunits. ADP also stimulates phosphorylation, without stimulating already phosphorylated catalytic subunit. ATP promotes dephosphorylation of catalytic subunit, rendering the AMPK enzyme inactive (By similarity).[UniProtKB/Swiss-Prot Function]