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Sarm1 (NM_001105817) Rat Tagged ORF Clone Lentiviral Particle
CAT＃: RR210840L3V
- LentiORF®
-
Lenti ORF particles, Sarm1 (Myc-DDK-tagged ORF) - Rat sterile alpha and TIR motif containing 1 (Sarm1), 200ul, >10^7 TU/mL
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CNY 12,065.00
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Specifications
| Product Data | |
| Product Name | Sarm1 (NM_001105817) Rat Tagged ORF Clone Lentiviral Particle |
| Vector | pLenti-C-Myc-DDK-P2A-Puro |
| ACCN | NM_001105817 |
| ORF Size | 2172 bp |
| Sequence Data |
The ORF insert of this clone is exactly the same as(RR210840).
|
| 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_001105817.1, NP_001099287.1 |
| RefSeq Size | 4039 bp |
| RefSeq ORF | 2175 bp |
| Locus ID | 287545 |
| Gene Summary | NAD(+) hydrolase, which plays a key role in axonal degeneration following injury by regulating NAD(+) metabolism. Acts as a negative regulator of MYD88- and TRIF-dependent toll-like receptor signaling pathway by promoting Wallerian degeneration, an injury-induced form of programmed subcellular death which involves degeneration of an axon distal to the injury site. Wallerian degeneration is triggered by NAD(+) depletion: in response to injury, SARM1 is activated and catalyzes cleavage of NAD(+) into ADP-D-ribose (ADPR), cyclic ADPR (cADPR) and nicotinamide; NAD(+) cleavage promoting cytoskeletal degradation and axon destruction. Also able to hydrolyze NADP(+), but not other NAD(+)-related molecules. Can activate neuronal cell death in response to stress. Regulates dendritic arborization through the MAPK4-JNK pathway. Involved in innate immune response: inhibits both TICAM1/TRIF- and MYD88-dependent activation of JUN/AP-1, TRIF-dependent activation of NF-kappa-B and IRF3, and the phosphorylation of MAPK14/p38.[UniProtKB/Swiss-Prot Function] |
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