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    recombinant-human-ctla4-protein-ab169909.pdf

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Immunology Adaptive Immunity T Cells Cytotoxic Cells
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Recombinant Human CTLA4 protein (ab169909)

  • Datasheet
  • SDS
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Key features and details

  • Expression system: Escherichia coli
  • Purity: > 90% SDS-PAGE
  • Tags: His-T7 tag N-Terminus
  • Suitable for: SDS-PAGE

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Description

  • Product name

    Recombinant Human CTLA4 protein
    See all CTLA4 proteins and peptides
  • Purity

    > 90 % SDS-PAGE.
    ab169909 was expressed in E.coli as inclusion bodies. The final product was refolded and chromatographically purified.
  • Expression system

    Escherichia coli
  • Accession

    P16410
  • Protein length

    Protein fragment
  • Animal free

    No
  • Nature

    Recombinant
    • Species

      Human
    • Sequence

      MASMTGGQQMGRGHHHHHHGNLYFQGGEFGKAMHVAQPAVVLASSRGIAS FVCEYASPGKATEV RVTVLRQADSQVTEVCAATYMMGNELTFLDDSIC TGTSSGNQVNLTIQGLRAMDTGLYICKVEL MYPPPYYLGIGNGTQIYV IDPEPCPDSD
    • Predicted molecular weight

      17 kDa including tags
    • Amino acids

      36 to 161
    • Tags

      His-T7 tag N-Terminus

Associated products

    Specifications

    Our Abpromise guarantee covers the use of ab169909 in the following tested applications.

    The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.

    • Applications

      SDS-PAGE

    • Form

      Liquid
    • Concentration information loading...

    Preparation and Storage

    • Stability and Storage

      Shipped at 4°C. Upon delivery aliquot and store at -80ºC. Avoid freeze / thaw cycles.

      pH: 8.00
      Constituent: 0.32% Tris HCl

      Contains NaCl, KCl, EDTA, arginine, DTT and glycerol.

    General Info

    • Alternative names

      • ALPS5
      • CD
      • CD 152
      • CD152
      • CD152 antigen
      • CD152 isoform
      • Celiac disease 3
      • CELIAC3
      • CTLA 4
      • CTLA-4
      • CTLA4
      • CTLA4_HUMAN
      • Cytotoxic T cell associated 4
      • Cytotoxic T lymphocyte antigen 4
      • Cytotoxic T lymphocyte associated 4
      • Cytotoxic T lymphocyte associated 4, soluble isoform, included
      • Cytotoxic T lymphocyte associated antigen 4
      • Cytotoxic T lymphocyte associated antigen 4 short spliced form
      • Cytotoxic T lymphocyte associated protein 4
      • Cytotoxic T lymphocyte associated serine esterase 4
      • Cytotoxic T lymphocyte protein 4
      • Cytotoxic T-lymphocyte protein 4
      • Cytotoxic T-lymphocyte-associated antigen 4
      • GRD4
      • GSE
      • ICOS
      • IDDM12
      • insulin-dependent diabetes mellitus 12
      • Ligand and transmembrane spliced cytotoxic T lymphocyte associated antigen 4
      • OTTHUMP00000216623
      see all
    • Function

      Inhibitory receptor acting as a major negative regulator of T-cell responses. The affinity of CTLA4 for its natural B7 family ligands, CD80 and CD86, is considerably stronger than the affinity of their cognate stimulatory coreceptor CD28.
    • Tissue specificity

      Widely expressed with highest levels in lymphoid tissues. Detected in activated T-cells where expression levels are 30- to 50-fold less than CD28, the stimulatory coreceptor, on the cell surface following activation.
    • Involvement in disease

      Genetic variation in CTLA4 influences susceptibility to systemic lupus erythematosus (SLE) [MIM:152700]. SLE is a chronic, inflammatory and often febrile multisystemic disorder of connective tissue. It affects principally the skin, joints, kidneys and serosal membranes. SLE is thought to represent a failure of the regulatory mechanisms of the autoimmune system.
      Note=Genetic variations in CTLA4 may influence susceptibility to Graves disease, an autoimmune disorder associated with overactivity of the thyroid gland and hyperthyroidism.
      Genetic variation in CTLA4 is the cause of susceptibility to diabetes mellitus insulin-dependent type 12 (IDDM12) [MIM:601388]. A multifactorial disorder of glucose homeostasis that is characterized by susceptibility to ketoacidosis in the absence of insulin therapy. Clinical fetaures are polydipsia, polyphagia and polyuria which result from hyperglycemia-induced osmotic diuresis and secondary thirst. These derangements result in long-term complications that affect the eyes, kidneys, nerves, and blood vessels.
      Genetic variation in CTLA4 is the cause of susceptibility to celiac disease type 3 (CELIAC3) [MIM:609755]. It is a multifactorial disorder of the small intestine that is influenced by both environmental and genetic factors. It is characterized by malabsorption resulting from inflammatory injury to the mucosa of the small intestine after the ingestion of wheat gluten or related rye and barley proteins. In its classic form, celiac disease is characterized in children by malabsorption and failure to thrive.
    • Sequence similarities

      Contains 1 Ig-like V-type (immunoglobulin-like) domain.
    • Post-translational
      modifications

      N-glycosylation is important for dimerization.
      Phosphorylation at Tyr-201 prevents binding to the AP-2 adapter complex, blocks endocytosis, and leads to retention of CTLA4 on the cell surface.
    • Cellular localization

      Cell membrane. Exists primarily an intracellular antigen whose surface expression is tightly regulated by restricted trafficking to the cell surface and rapid internalisation and.
    • Target information above from: UniProt accession P16410 The UniProt Consortium
      The Universal Protein Resource (UniProt) in 2010
      Nucleic Acids Res. 38:D142-D148 (2010) .

      Information by UniProt

    Protocols

    To our knowledge, customised protocols are not required for this product. Please try the standard protocols listed below and let us know how you get on.

    Click here to view the general protocols

    Datasheets and documents

    • SDS download

    • Datasheet download

      Download

    References (0)

    Publishing research using ab169909? Please let us know so that we can cite the reference in this datasheet.

    ab169909 has not yet been referenced specifically in any publications.

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