Ager (NM_007425) Mouse Tagged ORF Clone Lentiviral Particle

CAT#: MR206306L3V

  • LentiORF®

Lenti ORF particles, Ager (Myc-DDK-tagged) - Mouse advanced glycosylation end product-specific receptor (Ager), 200ul, >10^7 TU/mL

ORF Plasmid: DDK tGFP

Lentiviral Particles: DDK w/ Puro mGFP w/ Puro



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USD 1,236.00

7 Weeks*

Size
    • 200 ul

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Specifications

Product Data
Type Mouse Tagged ORF Clone
Tag Myc-DDK
Symbol Ager
Synonyms RAGE
Mammalian Cell Selection Puromycin
Vector pLenti-C-Myc-DDK-P2A-Puro
ACCN NM_007425
ORF Size 1209 bp
Sequence Data
The ORF insert of this clone is exactly the same as(MR206306).
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_007425.3, NP_031451.2
RefSeq Size 1387 bp
RefSeq ORF 1209 bp
Locus ID 11596
UniProt ID Q62151
Cytogenetics 17 B1
Gene Summary Mediates interactions of advanced glycosylation end products (AGE). These are nonenzymatically glycosylated proteins which accumulate in vascular tissue in aging and at an accelerated rate in diabetes. Acts as a mediator of both acute and chronic vascular inflammation in conditions such as atherosclerosis and in particular as a complication of diabetes. AGE/RAGE signaling plays an important role in regulating the production/expression of TNF-alpha, oxidative stress, and endothelial dysfunction in type 2 diabetes. Interaction with S100A12 on endothelium, mononuclear phagocytes, and lymphocytes triggers cellular activation, with generation of key proinflammatory mediators. Interaction with S100B after myocardial infarction may play a role in myocyte apoptosis by activating ERK1/2 and p53/TP53 signaling. Can also bind oligonucleotides. Receptor for amyloid beta peptide. Contributes to the translocation of amyloid-beta peptide (ABPP) across the cell membrane from the extracellular to the intracellular space in cortical neurons. ABPP-initiated RAGE signaling, especially stimulation of p38 mitogen-activated protein kinase (MAPK), has the capacity to drive a transport system delivering ABPP as a complex with RAGE to the intraneuronal space. RAGE-dependent signaling in microglia contributes to neuroinflammation, amyloid accumulation, and impaired learning/memory in a mouse model of Alzheimer disease.[UniProtKB/Swiss-Prot Function]

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