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Product Name
CARD9 antibody
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Description
CARD9 Rabbit Polyclonal antibody. Positive WB detected in PC-3 cells, HEK-293 cells, HL-60 cells, human placenta tissue. Observed molecular weight by Western-blot: 50-59kd
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Tested applications
ELISA, WB
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Species reactivity
Human,Mouse,Rat; other species not tested.
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Alternative names
CARD9 antibody; hCARD9 antibody
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Isotype
Rabbit IgG
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Preparation
This antibody was obtained by immunization of CARD9 recombinant protein (Accession Number: NM_052814). Purification method: Antigen affinity purified.
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Clonality
Polyclonal
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Formulation
PBS with 0.1% sodium azide and 50% glycerol pH 7.3.
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Storage instructions
Store at -20℃. DO NOT ALIQUOT
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Applications
Recommended Dilution:
WB: 1:200-1:2000
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Validations
PC-3 cells were subjected to SDS PAGE followed by western blot with Catalog No:108858(CARD9 antibody) at dilution of 1:500
HL-60 cells were subjected to SDS PAGE followed by western blot with Catalog No:108858(CARD9 antibody) at dilution of 1:300
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Background
CARD9, a member of the caspase recruitment domain (CARD) protein family, plays an important regulatory role in cell apoptosis. Defects in CARD9 are the cause of familial candidiasis type 2 (CANDF2) characterized by impaired clearance of fungal infections and results in colonization and infections of the mucosa or skin, predominantly with Candida albicans. CARD9 is highly expressed in spleen and regulate activation of NF-kappa-B by interaction with postive regulator of apoptosis BCL10 via the CARD domain.
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References
- Drewniak A, Gazendam RP, Tool AT. Invasive fungal infection and impaired neutrophil killing in human CARD9 deficiency. Blood. 121(13):2385-92. 2013.
- Herbst M, Gazendam R, Reimnitz D. Chronic Candida albicans Meningitis in a 4-Year-Old Girl with a Homozygous Mutation in the CARD9 Gene (Q295X). The Pediatric infectious disease journal. 34(9):999-1002. 2015.
- Drummond RA, Collar AL, Swamydas M. CARD9-Dependent Neutrophil Recruitment Protects against Fungal Invasion of the Central Nervous System. PLoS pathogens. 11(12):e1005293. 2015.
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