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The production of this recombinant Human SARM1 protein is just like all recombinant proteins. The process involved transfecting Baculovirus cells with DNA vector containing the template of recombinant DNA. The Baculovirus cells containing the template were then cultured so that they could transcribe and translate the SARM1 protein. N-terminal 10xHis tag and C-terminal Myc tag was used in the process. The purity is 0.85 determined by SDS-PAGE. Sterile alpha and toll/interleukin receptor motif-containing protein 1, SARM1, an executor of axonal degeneration, is an autoinhibitory NAD-consuming enzyme, composed of multiple domains. NMN and its analogs, CZ-48 and VMN, are the only known activators, which can release the inhibitory ARM domain from the enzymatic TIR domain. The later discovery that SARM1 promotes Wallerian degeneration suggested the existence of a pathway that might be targeted therapeutically. More recently, SARM1 was found to execute degeneration by hydrolyzing NAD+. Notably, SARM1 knockdown or knockout prevents neuron degeneration in response to a range of insults that lead to peripheral neuropathy, traumatic brain injury, and neurodegenerative disease. To be clarified, the reduction of cellular NAD+ concentration contributes to the disassembly of SARM1's peripheral ring, which allows formation of active NADase domain dimers, thereby further depleting NAD+ to cause an energetic catastrophe and cell death.
The production of this recombinant Human SARM1 protein is just like all recombinant proteins. The process involved transfecting Baculovirus cells with DNA vector containing the template of recombinant DNA. The Baculovirus cells containing the template were then cultured so that they could transcribe and translate the SARM1 protein. N-terminal 10xHis tag and C-terminal Myc tag was used in the process. The purity is 0.85 determined by SDS-PAGE. Sterile alpha and toll/interleukin receptor motif-containing protein 1, SARM1, an executor of axonal degeneration, is an autoinhibitory NAD-consuming enzyme, composed of multiple domains. NMN and its analogs, CZ-48 and VMN, are the only known activators, which can release the inhibitory ARM domain from the enzymatic TIR domain. The later discovery that SARM1 promotes Wallerian degeneration suggested the existence of a pathway that might be targeted therapeutically. More recently, SARM1 was found to execute degeneration by hydrolyzing NAD+. Notably, SARM1 knockdown or knockout prevents neuron degeneration in response to a range of insults that lead to peripheral neuropathy, traumatic brain injury, and neurodegenerative disease. To be clarified, the reduction of cellular NAD+ concentration contributes to the disassembly of SARM1’s peripheral ring, which allows formation of active NADase domain dimers, thereby further depleting NAD+ to cause an energetic catastrophe and cell death.
| Cat.No | ACP05200 | Target Name | Sarm1 |
|---|---|---|---|
| Form | Liquid or Lyophilized powder | Expression System | Baculovirus |
| Expression Range | 28-724aa | Mol Weight | 80.4 kDa |
| Protein Length | Full Length of Mature Protein | Purity | Greater than 85% as determined by SDS-PAGE. |
| Storage Buffer | 5%-50% glycerol. Lyophilized powder form: the buffer before lyophilization is Tris/PBS-based buffer, 6% Trehalose, Liquid form: default storage buffer is Tris/PBS-based buffer, pH 8.0. |
| Target Species | Human | Uniprot ID | Q6SZW1 |
|---|
Uniprot Id
Q6SZW1
Target Species
Human
Target Name
SARM1
Target Full Name
NAD(+) hydrolase SARM1
Target Function
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
Target Subcellular Location
Cytoplasm. Cell projection, axon. Cell projection, dendrite. Cell junction, synapse. Mitochondrion.
Target Tissue Specificity
Predominantly expressed in brain, kidney and liver. Expressed at lower level in placenta.
Target Research Area
Cell Biology
Target Synonyms
FLJ36296; KIAA0524; MyD88-5; SAM and ARM-containing protein; SAM domain-containing protein 2; SAMD2; SARM 1; SARM1; SARM1_HUMAN; Sterile alpha and Armadillo repeat protein; sterile alpha and HEAT/Armadillo motif protein; ortholog of Drosophila; sterile alpha and HEAT/Armadillo motifs-containing protein; sterile alpha and TIR motif containing 1; Sterile alpha and TIR motif-containing protein 1; Sterile alpha and TIR motifs-containing protein 1; Sterile alpha motif domain-containing protein 2; Tir-1 homolog
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