Anti-SARM1 Antibody (BSA and Azide free) (6174-11)
Our mouse SARM1 carrier-free monoclonal antibody from Antibodies Incorporated is produced in-house from clone 6174-11. It detects human, mouse, and rat SARM1 and is purified by Protein A chromatography. Works in WB, IHC, ICC, ELISA.
Human, Mouse, Rat
ELISA, ICC, IHC, WB
Mouse
SKU: 77-522-CF
Ships: 1-5 business days
Product Details
SARM1
SARM1 ( Sterile Alpha and TIR Motif-Containing 1) is predominantly expressed in the nervous system, particularly in neurons, and is highly conserved across different species. It encodes a protein that contains several functional domains, including a sterile alpha motif (SAM) domain, a Toll/interleukin-1 receptor (TIR) domain, and a catalytic domain with NAD^+ hydrolase activity.
SARM1 activation triggers a cascade of molecular events that leads to the breakdown of axonal structures and eventual degeneration.
In response to injury, SARM1 is activated and catalyzes cleavage of NAD+ into ADP-D-ribose (ADPR), cyclic ADPR (cADPR) and nicotinamide. In the nervous system, NAD+ depletion is a critical step in the axonal degeneration process, known as Wallerian degeneration, and is essential for clearing damaged axons to allow for regeneration and repair. Inhibition of SARM1 or the preservation of NAD+ levels has been shown to protect axons from degeneration in experimental models, suggesting SARM1 as a potential therapeutic target for neurodegenerative diseases and nerve injuries.
Research on SARM1 has primarily focused on its role in axonal degeneration and neuroprotection. Understanding the molecular mechanisms underlying SARM1 activation and its downstream effects may have implications for developing treatments for various neurological disorders, such as peripheral neuropathies, traumatic brain injury, and neurodegenerative diseases like Parkinson's and Alzheimer's.
Purified by Protein A chromatography
Lot dependent: provided at 0.6-1.0 mg/mL
Monoclonal
6174-11
IgG2b
ELISA, ICC, IHC, WB
Mouse
SARM1
73 kDa
Fusion protein amino acids 51-724 of human SARM1 (accession number Q6SZW1) produced recombinantly in E. Coli.
Human
Human, Mouse, Rat
Aliquot and store at ≤ -20°C for long term storage. For short term storage, store at 2-8°C. For maximum recovery of product, centrifuge the vial prior to removing the cap.
Liquid
Produced by in vitro bioreactor culture of hybridoma line followed by Protein A affinity chromatography and buffer exchanged into 1X PBS. Purified mAbs are >90% specific antibody.
PBS
Unconjugated
No cross-reactivity reported
Each new lot of antibody is quality control tested by western blot on rat whole brain lysate and confirmed to stain the expected molecular weight band.
These antibodies are to be used as research laboratory reagents and are not for use as diagnostic or therapeutic reagents in humans.
United States
12 months from date of receipt
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
Q6SZW1
UniProt 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.
UniProt 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.
23098
Shipped on ice packs

