Misfolded Human SOD1 Mouse Monoclonal Antibody - Purified | FR | MédiMabs

Misfolded Human SOD1 Mouse Monoclonal Antibody - Purified

Misfolded Human SOD1 Mouse Monoclonal Antibody - Purified

  • Misfolded Human SOD1 Mouse Monoclonal Antibody - Purified

Misfolded Human SOD1 Mouse Monoclonal Antibody - Purified

MM-0070-3-P
$500,00/200 µl
QTY
Pour les prix de gros, nous contacter.
NUMÉRO : MM-0070-3-P
  • Nom du produit
    Misfolded Human SOD1 Mouse Monoclonal Antibody - Purified
  • Serveur
    Mouse
  • Clonality
    Monoclonal
  • Tested Applications
    Western Blot (WB), Immunoprecipitation (IP), Immunofluorescence (IF)
  • Research Area(s)
    Neuroscience, Signal Transduction, Cell Biology, Cancer, Metabolism
  • Immunogen
    Recombinant human SOD1 G93A APO
  • Modifications
    None
  • Clone ID
    A5C3
  • DataSHEET
  • Isotype
    IgG1
  • Conjugation
    None
  • Reactivity
    The antibody recognizes misfolded forms of mutant human SOD1 protein. IF: G93A, G85R, and G37R; WB (denatured): G93A, G127X and G37R; WB (native): G37R; IP: G93A, G127X and G37R.
  • Specificity
    Human and Mouse
  • Purification
    Protein G
  • Target Name
    human SOD1 mutant protein
  • Storage Buffer
    PBS
  • Alias
    Superoxide dismutase [Cu-Zn], Superoxide dismutase 1, hSOD1, SOD1
  • Format
    200 µl
  • Background
    Superoxide dismutase 1 (SOD1) is a soluble cytoplasmic and mitochondrial intermembrane space protein. SOD1 binds copper and zinc ions and is one of three isozymes responsible for destroying free superoxide radicals in the body. Mutations in SOD1 cause familial amyotrophic lateral sclerosis type 1 (ALS1). These mutations have been linked to accumulation of harmful superoxide radicals, promotion of apoptosis, formation of aggregates of misfolded superoxide dismutase which are toxic and the continued stimulation of nerve cells that causes them to burn out and die.

For laboratory research only, not for drug, diagnostic or other use.

  • Oral Treatment with CuII(atsm) Increases Mutant SOD1 In Vivo but Protects Motor Neurons and Improves the Phenotype of a Transgenic Mouse Model of Amyotrophic Lateral Sclerosis
  • Enhancing Mitochondrial Calcium Buffering Capacity Reduces Aggregation of Misfolded SOD1 and Motor Neuron Cell Death without Extending Survival in Mouse Models of
  • Replacement of microglial cells using Clodronate liposome and bone marrow transplantation in the central nervous system of SOD1G93A transgenic mice as an in vivo model of amyotrophic lateral sclerosis
  • Methylene Blue Administration Fails to Confer Neuroprotection in Two Amyotrophic Lateral Sclerosis Mouse Models
  • Misfolded SOD1 Associated with Motor Neuron Mitochondria Alters Mitochondrial Shape and Distribution Prior to Clinical Onset
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