Product nameAnti-IL-12 p40 antibody
See all IL-12 p40 primary antibodies
DescriptionRabbit polyclonal to IL-12 p40
Tested applicationsSuitable for: WB, ELISAmore details
Species reactivityReacts with: Chicken
Does not react with: Cow
Recombinant full length protein corresponding to Chicken IL-12 p40 aa 20-315.
AQWKLRENVY VIESEWNDET PAKKVKLTCD TSDEALPVYW KKGTELKGTG KTLTTEVKEF PDAGNYTCLS AKTHEIISYS FFLITKVDSN GQMIRSILKS YKEPSKTFLK CEAKNYSGIF TCSWMTENES PSVKFTIRSL KGSQGDVTCS SPVARTDKSV TEYTAQCQKE NYCPFAEEHQ PTEMFLEVID EVEYENYTSS FFIRDIIKPD PPQCQYASTN GTVTWTYPKT WSTPKSYFPL TFRVKVESTK KYKSKVYDAD EQSIQIPKTG PKDKISVQAR DRYYNSSWSE WSTLCR
Database link: 404671
Cross-reactivity determined in ELISA
Storage instructionsShipped at 4°C. Store at +4°C short term (1-2 weeks). Upon delivery aliquot. Store at -20°C long term. Avoid freeze / thaw cycle.
Storage bufferPreservative: 0.09% Sodium azide
Constituent: 99% PBS
Concentration information loading...
PurityImmunogen affinity purified
Our Abpromise guarantee covers the use of ab193854 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|WB||Use a concentration of 0.1 - 1 µg/ml. Predicted molecular weight: 36 kDa.|
|ELISA||Use a concentration of 0.5 - 5 µg/ml.|
FunctionCytokine that can act as a growth factor for activated T and NK cells, enhance the lytic activity of NK/lymphokine-activated killer cells, and stimulate the production of IFN-gamma by resting PBMC.
Associates with IL23A to form the IL-23 interleukin, an heterodimeric cytokine which functions in innate and adaptive immunity. IL-23 may constitute with IL-17 an acute response to infection in peripheral tissues. IL-23 binds to an heterodimeric receptor complex composed of IL12RB1 and IL23R, activates the Jak-Stat signaling cascade, stimulates memory rather than naive T-cells and promotes production of proinflammatory cytokines. IL-23 induces autoimmune inflammation and thus may be responsible for autoimmune inflammatory diseases and may be important for tumorigenesis.
Involvement in diseaseDefects in IL12B are a cause of mendelian susceptibility to mycobacterial disease (MSMD) [MIM:209950]; also known as familial disseminated atypical mycobacterial infection. This rare condition confers predisposition to illness caused by moderately virulent mycobacterial species, such as Bacillus Calmette-Guerin (BCG) vaccine and environmental non-tuberculous mycobacteria, and by the more virulent Mycobacterium tuberculosis. Other microorganisms rarely cause severe clinical disease in individuals with susceptibility to mycobacterial infections, with the exception of Salmonella which infects less than 50% of these individuals. The pathogenic mechanism underlying MSMD is the impairment of interferon-gamma mediated immunity, whose severity determines the clinical outcome. Some patients die of overwhelming mycobacterial disease with lepromatous-like lesions in early childhood, whereas others develop, later in life, disseminated but curable infections with tuberculoid granulomas. MSMD is a genetically heterogeneous disease with autosomal recessive, autosomal dominant or X-linked inheritance.
Genetic variations in IL12B are a cause of susceptibility to psoriasis type 11 (PSORS11) [MIM:612599]. Psoriasis is a common, chronic inflammatory disease of the skin with multifactorial etiology. It is characterized by red, scaly plaques usually found on the scalp, elbows and knees. These lesions are caused by abnormal keratinocyte proliferation and infiltration of inflammatory cells into the dermis and epidermis.
Sequence similaritiesBelongs to the type I cytokine receptor family. Type 3 subfamily.
Contains 1 fibronectin type-III domain.
Contains 1 Ig-like C2-type (immunoglobulin-like) domain.
modificationsKnown to be C-mannosylated in the recombinant protein; it is not yet known for sure if the wild-type protein is also modified.
- Information by UniProt
- CLMF antibody
- CLMF p40 antibody
- CLMF2 antibody
ab193854 has not yet been referenced specifically in any publications.