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AB169623

Anti-CARD9 antibody

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(2 Publications)

Mouse Polyclonal CARD9 antibody. Suitable for WB, ICC/IF and reacts with Human samples. Cited in 2 publications. Immunogen corresponding to Recombinant Full Length Protein corresponding to Human CARD9.

View Alternative Names

Caspase recruitment domain-containing protein 9, hCARD9, CARD9

2 Images
Immunocytochemistry/ Immunofluorescence - Anti-CARD9 antibody (AB169623)
  • ICC/IF

Unknown

Immunocytochemistry/ Immunofluorescence - Anti-CARD9 antibody (AB169623)

Immunofluorescent analysis of HeLa cells labeling CARD9 with ab169623 at 10 µg/ml.

Western blot - Anti-CARD9 antibody (AB169623)
  • WB

Unknown

Western blot - Anti-CARD9 antibody (AB169623)

All lanes:

Western blot - Anti-CARD9 antibody (ab169623) at 1 µg/mL

Lane 1:

CARD9 transfected 293T cell lysate at 15 µL

Lane 2:

Non-transfected 293T cell lysate at 15 µL

Predicted band size: 58 kDa,617 kDa,62 kDa,66 kDa

Observed band size: 58 kDa,65 kDa

true

Key facts

Host species

Mouse

Clonality

Polyclonal

Isotype

IgG

Carrier free

No

Reacts with

Human

Applications

ICC/IF, WB

applications

Immunogen

Recombinant Full Length Protein corresponding to Human CARD9.

Q9H257

Reactivity data

{ "title": "Reactivity Data", "filters": { "stats": ["", "Species", "Dilution Info", "Notes"], "tabs": { "all-applications": {"fullname" : "All Applications", "shortname": "All Applications"}, "WB" : {"fullname" : "Western blot", "shortname":"WB"}, "ICCIF" : {"fullname" : "Immunocytochemistry/ Immunofluorescence", "shortname":"ICC/IF"} }, "product-promise": { "all": "all", "testedAndGuaranteed": "tested", "guaranteed": "expected", "predicted": "predicted", "notRecommended": "not-recommended" } }, "values": { "Human": { "WB-species-checked": "testedAndGuaranteed", "WB-species-dilution-info": "1 µg/mL", "WB-species-notes": "<p></p>", "ICCIF-species-checked": "testedAndGuaranteed", "ICCIF-species-dilution-info": "10 µg/mL", "ICCIF-species-notes": "<p></p>" } } }

Properties and storage information

Form
Liquid
Purification technique
Affinity purification Protein A
Storage buffer
pH: 7.4 Constituents: PBS
Shipped at conditions
Blue Ice
Appropriate short-term storage duration
1-2 weeks
Appropriate short-term storage conditions
+4°C
Appropriate long-term storage conditions
-20°C
Aliquoting information
Upon delivery aliquot

Supplementary information

This supplementary information is collated from multiple sources and compiled automatically.

CARD9 also known as Caspase Recruitment Domain Family Member 9 is a signaling protein that plays a critical role in immune cell function. It has a molecular mass of approximately 59 kDa. CARD9 is primarily expressed in myeloid cells including dendritic cells monocytes and macrophages. Its mechanical function involves acting as an adaptor protein in immune signaling pathways allowing it to mediate the interaction between upstream pattern recognition receptors and downstream kinases.
Biological function summary

CARD9 is instrumental in the activation of the immune system’s response to pathogens such as fungi and bacteria. It functions as part of the CARD-Bcl10-MALT1 signaling complex which triggers the activation of NF-kB a transcription factor essential for inflammatory responses. Through its role in this complex CARD9 ensures the regulation of cytokine production which is fundamental for effective immune responses. CARD9's activity supports the defense against pathogenic infections by facilitating communication in immune signaling.

Pathways

CARD9 is involved in critical immune response pathways including the C-type lectin receptor (CLR) pathway. This pathway is essential in recognizing fungal pathogens and initiating immune responses. CARD9 interacts with proteins like Syk and Bcl10 in the CLR pathway to propagate immune signaling. CARD9's role in these pathways highlights its significance in regulating immune activities and maintaining homeostasis through signaling cascades.

CARD9 deficiency can result in impaired immune responses leading to increased susceptibility to fungal infections such as candidiasis. The protein plays an important role in maintaining appropriate immune functions to prevent such conditions. Furthermore dysfunction in CARD9 signaling has been associated with inflammatory bowel diseases. In this context CARD9 interacts with other immune proteins like NOD2 to modulate intestinal inflammation. Understanding CARD9’s role helps in elucidating its potential as a therapeutic target for managing these diseases.

Product protocols

For this product, it's our understanding that no specific protocols are required. You can visit:

Target data

Adapter protein that plays a key role in innate immune response against fungi by forming signaling complexes downstream of C-type lectin receptors (PubMed : 26961233, PubMed : 33558980). CARD9-mediated signals are essential for antifungal immunity against a subset of fungi from the phylum Ascomycota (PubMed : 24231284, PubMed : 25057046, PubMed : 25702837, PubMed : 26521038, PubMed : 26679537, PubMed : 26961233, PubMed : 27777981, PubMed : 29080677, PubMed : 33558980). Transduces signals in myeloid cells downstream of C-type lectin receptors CLEC7A (dectin-1), CLEC6A (dectin-2) and CLEC4E (Mincle), which detect pathogen-associated molecular pattern metabolites (PAMPs), such as fungal carbohydrates, and trigger CARD9 activation (By similarity). Upon activation, CARD9 homooligomerizes to form a nucleating helical template that recruits BCL10 via CARD-CARD interaction, thereby promoting polymerization of BCL10 and subsequent recruitment of MALT1 : this leads to activation of NF-kappa-B and MAP kinase p38 (MAPK11, MAPK12, MAPK13 and/or MAPK14) pathways which stimulate expression of genes encoding pro-inflammatory cytokines and chemokines (PubMed : 11053425, PubMed : 26488816, PubMed : 26961233, PubMed : 31296852, PubMed : 33558980). CARD9 signaling in antigen-presenting cells links innate sensing of fungi to the activation of adaptive immunity and provides a cytokine milieu that induces the development and subsequent of interleukin 17-producing T helper (Th17) cells (PubMed : 24231284). Also involved in activation of myeloid cells via classical ITAM-associated receptors and TLR : required for TLR-mediated activation of MAPK, while it is not required for TLR-induced activation of NF-kappa-B (By similarity). CARD9 can also be engaged independently of BCL10 : forms a complex with RASGRF1 downstream of C-type lectin receptors, which recruits and activates HRAS, leading to ERK activation and the production of cytokines (By similarity). Acts as an important regulator of the intestinal commensal fungi (mycobiota) component of the gut microbiota (PubMed : 33548172). Plays an essential role in antifungal immunity against dissemination of gut fungi : acts by promoting induction of antifungal IgG antibodies response in CX3CR1(+) macrophages to confer protection against disseminated C.albicans or C.auris infection (PubMed : 33548172). Also mediates immunity against other pathogens, such as certain bacteria, viruses and parasites; CARD9 signaling is however redundant with other innate immune responses (By similarity). In response to L.monocytogenes infection, required for the production of inflammatory cytokines activated by intracellular peptidoglycan : acts by connecting NOD2 recognition of peptidoglycan to downstream activation of MAP kinases (MAPK) without activating NF-kappa-B (By similarity).
See full target information CARD9

Publications (2)

Recent publications for all applications. Explore the full list and refine your search

Journal of physiological anthropology 39:32 PubMed33028417

2020

NOD-like receptors mediate inflammatory lung injury during plateau hypoxia exposure.

Applications

Unspecified application

Species

Unspecified reactive species

Haiyan Wang,Xue Lin,Xiaoyan Pu

Molecular medicine reports 16:6013-6019 PubMed28849138

2017

Construction of a lentiviral vector containing shRNA targeting ADAM17 and its role in attenuating endotoxemia in mice.

Applications

Unspecified application

Species

Unspecified reactive species

Bing He,Xiaoou Li,Tuo Hu,Wenjing Lian,Mingxia Zhang
View all publications

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