Biotinylated Human CTLA-4 Protein, His,Avitag™

Proteins and Peptides

貨號 Cat. No.
CT4-H82E1
規格 Size
200ug
品牌 Brand
ACROBiosystems
Species
Human
Conjugate
Precision Avi
Expression System
HEK293
Tag
Avi Tag 、 His Tag

Description




Source : 


Biotinylated Human CTLA-4, His,Avitag (CT4-H82E1) is expressed from human 293 cells (HEK293). It contains AA Ala 37 - Phe 162 (Accession # Q6GR94-1).


 

Molecule : CTLA-4


 

Synonyms : CTLA4,CD152


 

Format : Powder


 

Category : MABSol® Biotin Labeled Proteins


 

Accession : NP_005205.2


 

Storage : -20℃


 

Shipping condition : Powder,RT


 

Molecular Weight : 17.2 kDa


 

Characteristics :


This protein carries a polyhistidine tag at the C-terminus, followed by an Avi tag. The protein has a calculated MW of 17.2 kDa. The protein migrates as 22-30 kDa under reducing (R) condition (SDS-PAGE) due to glycosylation.


 

Endotoxin Level : Less than 1.0 EU per μg by the LAL method.


 

Buffer : PBS, pH7.4


 

Description :


CTLA-4 (Cytotoxic T-Lymphocyte Antigen 4) is also known as CD152 (Cluster of differentiation 152), is a protein receptor that downregulates the immune system. CTLA4 is a member of the immunoglobulin superfamily, which is expressed on the surface of Helper T cells and transmits an inhibitory signal to T cells. The protein contains an extracellular V domain, a transmembrane domain, and a cytoplasmic tail. Alternate splice variants, encoding different isoforms. CTLA4 is similar to the T-cell co-stimulatory protein, CD28, and both molecules bind to CD80 and CD86, also called B7-1 and B7-2 respectively, on antigen-presenting cells. CTLA4 transmits an inhibitory signal to T cells, whereas CD28 transmits a stimulatory signal. Intracellular CTLA4 is also found in regulatory T cells and may be important to their function. Fusion proteins of CTLA4 and antibodies (CTLA4-Ig) have been used in clinical trials for rheumatoid arthritis.


 

References :


(1) Waterhouse P, et al., 1995, Science 270 (5238): 985–8.
(2) Magistrelli G, et al., 1999. Eur. J. Immunol. 29 (11): 3596–602.
(3) Rudd, CE. et al., 2009, Immunol. Rev. 229 (1): 12-26.





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