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SH2D1A recombinant protein

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Catalog # MBS203869
Unit / Price
  0.1 mg  /  $310 +1 FREE 8GB USB
  0.5 mg  /  $720 +1 FREE 8GB USB
SDS-Page
Product Name

SH2D1A, Recombinant Protein

Popular Item
Full Product Name

SH2D1A, 1-128aa, Human, His tag, E Coli

Product Synonym Names
SH2 domain-containing protein 1A; DSHP; EBVS; IMD5; LYP; MTCP1; SAP; XLP; XLPD
Research Use Only
For Research Use Only. Not for use in diagnostic procedures.
Sequence
MGSSHHHHHH SSGLVPRGSH MDAVAVYHGK ISRETGEKLL LATGLDGSYL LRDSESVPGV YCLCVLYHGY IYTYRVSQTE TGSWSAETAP GVHKRYFRKI KNLISAFQKP DQGIVIPLQY PVEKKSSARS TQGTTGIRED PDVCLKAP
OMIM
AL023657 mRNA
3D Structure
ModBase 3D Structure for O60880
Host
E Coli
Purity/Purification
> 95% by SDS-PAGE
Form/Format
Liquid. In 20 mM Tris-HCl Buffer (pH 7.5) containing 1 mM DTT, 10% glycerol
Concentration
1mg/ml (determined by Bradford assay) (lot specific)
Antigen Species
Human
Tag Information
His-tag
Preparation and Storage
Can be stored at 4 degree C short term (1-2 weeks).
For long term storage, aliquot and store at -20 degree C or -70 degree C.
Avoid repeated freezing and thawing cycles.
Other Notes
Small volumes of SH2D1A recombinant protein vial(s) may occasionally become entrapped in the seal of the product vial during shipment and storage. If necessary, briefly centrifuge the vial on a tabletop centrifuge to dislodge any liquid in the container`s cap. Certain products may require to ship with dry ice and additional dry ice fee may apply.
Related Product Information for
SH2D1A recombinant protein
SH2D1A is an inhibitor of the signaling lymphocyte activation molecule (SLAM) self-association. This protein is expressed at a high level in thymus and lung, with a lower level of expression in spleen and liver. Defects in SH2D1A are a cause of X-linked lymphoproliferative disease (XLPD) also known as Duncan disease. XLPD is characterized by a rare congenital immunodeficiency following Epstein-Barr virus (EBV) infection. Recombinant human SH2D1A protein, fused to His-tag at N-terminus, was expressed in E Coli and purified by using conventional chromatography.
Product Categories/Family for SH2D1A recombinant protein
Applications Tested/Suitable for SH2D1A recombinant protein
SDS-PAGE

NCBI/Uniprot data below describe general gene information for SH2D1A. It may not necessarily be applicable to this product.
NCBI GI #
NCBI GeneID
NCBI Accession #
NCBI GenBank Nucleotide #
UniProt Primary Accession #
UniProt Secondary Accession #
UniProt Related Accession #
Molecular Weight
16.3 kDa (148aa), confirmed by MALDI-TOF
NCBI Official Full Name
SH2 domain-containing protein 1A isoform 1
NCBI Official Synonym Full Names
SH2 domain containing 1A
NCBI Official Symbol
SH2D1A  [Similar Products]
NCBI Official Synonym Symbols
LYP; SAP; XLP; DSHP; EBVS; IMD5; XLPD; MTCP1; XLPD1; SAP/SH2D1A
  [Similar Products]
NCBI Protein Information
SH2 domain-containing protein 1A
UniProt Protein Name
SH2 domain-containing protein 1A
UniProt Synonym Protein Names
Duncan disease SH2-protein; Signaling lymphocytic activation molecule-associated protein; SLAM-associated protein; T-cell signal transduction molecule SAP
UniProt Gene Name
SH2D1A  [Similar Products]
UniProt Synonym Gene Names
DSHP; SAP; SLAM-associated protein  [Similar Products]
NCBI Summary for SH2D1A
This gene encodes a protein that plays a major role in the bidirectional stimulation of T and B cells. This protein contains an SH2 domain and a short tail. It associates with the signaling lymphocyte-activation molecule, thereby acting as an inhibitor of this transmembrane protein by blocking the recruitment of the SH2-domain-containing signal-transduction molecule SHP-2 to its docking site. This protein can also bind to other related surface molecules that are expressed on activated T, B and NK cells, thereby modifying signal transduction pathways in these cells. Mutations in this gene cause lymphoproliferative syndrome X-linked type 1 or Duncan disease, a rare immunodeficiency characterized by extreme susceptibility to infection with Epstein-Barr virus, with symptoms including severe mononucleosis and malignant lymphoma. Multiple transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Jul 2008]
UniProt Comments for SH2D1A
Cytoplasmic adapter regulating receptors of the signaling lymphocytic activation molecule (SLAM) family such as SLAMF1, CD244, LY9, CD84, SLAMF6 and SLAMF7. In SLAM signaling seems to cooperate with SH2D1B/EAT-2. Initially it has been proposed that association with SLAMF1 prevents SLAMF1 binding to inhibitory effectors including INPP5D/SHIP1 and PTPN11/SHP-2 (PubMed:11806999). However, by simultaneous interactions, recruits FYN which subsequently phosphorylates and activates SLAMF1 (PubMed:12458214). Positively regulates CD244/2B4- and CD84-mediated natural killer (NK) cell functions. Can also promote CD48-, SLAMF6 -, LY9-, and SLAMF7-mediated NK cell activation. In the context of NK cell-mediated cytotoxicity enhances conjugate formation with target cells (). May also regulate the activity of the neurotrophin receptors NTRK1, NTRK2 and NTRK3.
Product References and Citations for SH2D1A recombinant protein
Schwartzberg PL., et al. (2010) Immunity. 32 (2):253-65.; Lenardo MJ., et al (2009) J Clin Invest. 119 (10):2976-89;

Precautions
All of MyBioSource's Products are for scientific laboratory research purposes and are not for diagnostic, therapeutics, prophylactic or in vivo use. Through your purchase, you expressly represent and warrant to MyBioSource that you will properly test and use any Products purchased from MyBioSource in accordance with industry standards. MyBioSource and its authorized distributors reserve the right to refuse to process any order where we reasonably believe that the intended use will fall outside of our acceptable guidelines.
Disclaimer
While every efforts were made to ensure the accuracy of the information provided in this datasheet, MyBioSource will not be liable for any omissions or errors contained herein. MyBioSource reserves the right to make changes to this datasheet at any time without prior notice.

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