Rabbit Polyclonal SARM antibody. Suitable for IHC-P and reacts with Human samples. Cited in 2 publications. Immunogen corresponding to Synthetic Peptide within Human SARM1 conjugated to Keyhole Limpet Haemocyanin.
pH: 7.4
Preservative: 0.02% Sodium azide
Constituents: 99% PBS
IHC-P | |
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Human | Tested |
Species | Dilution info | Notes |
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Species Human | Dilution info 2.00000-10.00000 µg/mL | Notes Perform heat-mediated antigen retrieval with citrate buffer pH 6 before commencing with IHC staining protocol. |
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NAD(+) hydrolase, which plays a key role in axonal degeneration following injury by regulating NAD(+) metabolism (PubMed:25908823, PubMed:27671644, PubMed:28334607). 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 (PubMed:15123841, PubMed:16964262, PubMed:20306472, PubMed:25908823). 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 (PubMed:25908823, PubMed:28334607, PubMed:30333228, PubMed:31128467, PubMed:31439792, PubMed:31439793, PubMed:32049506, PubMed:32828421, PubMed:33053563). Also able to hydrolyze NADP(+), but not other NAD(+)-related molecules (PubMed:29395922). Can activate neuronal cell death in response to stress (PubMed:20306472). Regulates dendritic arborization through the MAPK4-JNK pathway (By similarity). 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 (PubMed:16964262).
KIAA0524, SAMD2, SARM, SARM1, NAD(+) hydrolase SARM1, NADase SARM1, hSARM1, NADP(+) hydrolase SARM1, Sterile alpha and Armadillo repeat protein, Sterile alpha and TIR motif-containing protein 1, Sterile alpha motif domain-containing protein 2, Tir-1 homolog, MyD88-5, SAM domain-containing protein 2, HsTIR
Rabbit Polyclonal SARM antibody. Suitable for IHC-P and reacts with Human samples. Cited in 2 publications. Immunogen corresponding to Synthetic Peptide within Human SARM1 conjugated to Keyhole Limpet Haemocyanin.
pH: 7.4
Preservative: 0.02% Sodium azide
Constituents: 99% PBS
The sterile alpha and HEAT/Armadillo motif-containing protein commonly known as SARM is a member of the death domain superfamily. It has a molecular mass of approximately 68 kDa. SARM is expressed in the nervous system and various immune cells. Mechanically SARM functions as an adaptor protein involved in signaling pathways related to immunity and neuroprotection. It primarily modulates signaling cascades by interacting with other key proteins within the cellular environment.
SARM engages in processes that are important to maintaining neurological health and regulating immune responses. It serves as a part of the innate immunity complex where it contributes to the regulation of inflammatory responses. SARM can also influence mitochondrial function indicating it plays a significant role in cellular energy management and apoptosis control. These multifaceted functions highlight its engagement in complex and dynamic cellular processes.
SARM plays an important role in the toll-like receptor (TLR) signaling pathway and mitochondrial apoptosis pathway. SARM interacts closely with TLRs to modulate immune responses particularly impacting the production of type I interferons. In the mitochondrial apoptosis pathway SARM relates to proteins like TRAF6 impacting cell death and survival. Its involvement in these pathways reflects its essential function in controlling cellular stress responses.
SARM has been implicated in neurological diseases such as Alzheimer's disease and infectious diseases such as viral encephalitis. In Alzheimer's disease SARM interacts with other proteins like amyloid precursor protein (APP) modulating pathways that may exacerbate neurodegeneration. In viral encephalitis SARM mediates immune responses providing a link to immune-related proteins like MyD88 which contribute to neuronal damage during infection. This makes SARM a target of interest for therapeutic interventions in both neurological and infectious diseases.
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ab115561, at 2µg/ml, staining SARM in Formalin-fixed, Paraffin-embedded Human Tonsil tissue by Immunohistochemistry followed by biotinylated secondary antibody, alkaline phosphatase-streptavidin and chromogen.
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