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SARM1 / SARM Antibody (clone Sarmy-1)

Mouse Monoclonal Antibody

     
  • IHC - SARM1 / SARM Antibody (clone Sarmy-1) ALS11212
    Anti-SARM1 / SARM antibody IHC of human brain, cortex.
  • SPECIFICATION
  • CITATIONS
  • PROTOCOLS
  • BACKGROUND
Product Information
Application
  • Applications Legend:
  • WB=Western Blot
  • IHC=Immunohistochemistry
  • IHC-P=Immunohistochemistry (Paraffin-embedded Sections)
  • IHC-F=Immunohistochemistry (Frozen Sections)
  • IF=Immunofluorescence
  • FC=Flow Cytopmetry
  • IC=Immunochemistry
  • ICC=Immunocytochemistry
  • E=ELISA
  • IP=Immunoprecipitation
  • DB=Dot Blot
  • CHIP=Chromatin Immunoprecipitation
  • FA=Fluorescence Assay
  • IEM=Immunoelectronmicroscopy
  • EIA=Enzyme Immunoassay
IHC-P, IP
Primary Accession Q6SZW1
Reactivity Human
Host Mouse
Clonality Monoclonal
Clone Names Sarmy-1
Calculated MW 79kDa
Dilution IHC-P (10 µg/ml), IP (1:200),
Additional Information
Gene ID 23098
Other Names Sterile alpha and TIR motif-containing protein 1, Sterile alpha and Armadillo repeat protein, Sterile alpha motif domain-containing protein 2, MyD88-5, SAM domain-containing protein 2, Tir-1 homolog, SARM1, KIAA0524, SAMD2, SARM
Target/Specificity Recognizes human SARM.
Reconstitution & Storage Long term: -70°C; Short term: +4°C
PrecautionsSARM1 / SARM Antibody (clone Sarmy-1) is for research use only and not for use in diagnostic or therapeutic procedures.
Protein Information
Name SARM1
Synonyms KIAA0524, SAMD2, SARM
Function Negative regulator of MYD88- and TRIF-dependent toll- like receptor signaling pathway which plays a pivotal role in activating axonal degeneration following injury. Promotes Wallerian degeneration an injury-induced axonal death pathway which involves degeneration of an axon distal to the injury site. Can activate neuronal 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.
Cellular Location Cytoplasm. Cell projection, axon. Cell projection, dendrite. Cell junction, synapse. Mitochondrion. Note=Associated with microtubules.
Tissue Location Predominantly expressed in brain, kidney and liver. Expressed at lower level in placenta
Research Areas
Citations (0)

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Background

Negative regulator of MYD88- and TRIF-dependent toll- like receptor signaling pathway which plays a pivotal role in activating axonal degeneration following injury. Promotes Wallerian degeneration an injury-induced axonal death pathway which involves degeneration of an axon distal to the injury site. Can activate neuronal 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.

References

Mink M.,et al.Genomics 74:234-244(2001).
Bousson J.-C.,et al.Submitted (OCT-2003) to the EMBL/GenBank/DDBJ databases.
Nagase T.,et al.DNA Res. 5:31-39(1998).
Liberati N.T.,et al.Proc. Natl. Acad. Sci. U.S.A. 101:6593-6598(2004).
Carty M.,et al.Nat. Immunol. 7:1074-1081(2006).

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$ 395.00
Cat# ALS11212
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