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Mouse Anti-CARD14 Recombinant Antibody (CBXC-0067) (CBMAB-C5715-CQ)

This product is a mouse antibody that recognizes CARD14. The antibody CBXC-0067 can be used for immunoassay techniques such as: S-ELISA, ELISA.
See all CARD14 antibodies

Summary

Host Animal
Mouse
Specificity
Human
Clone
CBXC-0067
Antibody Isotype
IgG2b, κ
Application
S-ELISA, ELISA

Basic Information

Immunogen
CARD14 (NP_077015, 905 a.a.-1004 a.a) partial recombinant protein with GST tag.
Specificity
Human
Antibody Isotype
IgG2b, κ
Clonality
Monoclonal
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

Formulations & Storage [For reference only, actual COA shall prevail!]

Format
Liquid
Buffer
PBS, pH 7.4
Concentration
0.5 mg/mL
Storage
Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freeze/thaw cycles.

Target

Full Name
Caspase Recruitment Domain Family Member 14
Introduction
CARD14 (Caspase Recruitment Domain Family Member 14) is a Protein Coding gene. Diseases associated with CARD14 include Pityriasis Rubra Pilaris and Psoriasis 2. Among its related pathways are NF-KappaB Family Pathway and NF-kappa B signaling pathway. Gene Ontology (GO) annotations related to this gene include CARD domain binding. An important paralog of this gene is CARD11.
Entrez Gene ID
79092
UniProt ID
Q9BXL6
Alternative Names
Caspase Recruitment Domain Family Member 14; CARD-Containing MAGUK Protein 2; CARMA2; Caspase Recruitment Domain-Containing Protein 14; Caspase Recruitment Domain Family, Member 14; Bcl10-Interacting Maguk Protein 2; Psoriasis Susceptibility 2;
Function
Acts as a scaffolding protein that can activate the inflammatory transcription factor NF-kappa-B and p38/JNK MAP kinase signaling pathways. Forms a signaling complex with BCL10 and MALT1, and activates MALT1 proteolytic activity and inflammatory gene expression. MALT1 is indispensable for CARD14-induced activation of NF-kappa-B and p38/JNK MAP kinases (PubMed:11278692, PubMed:21302310, PubMed:27113748, PubMed:27071417).
May play a role in signaling mediated by TRAF2, TRAF3 and TRAF6 and protects cells against apoptosis.
Isoform 3: Not able to activate the inflammatory transcription factor NF-kappa-B and may function as a dominant negative regulator (PubMed:21302310, PubMed:26358359).
Biological Process
Activation of NF-kappaB-inducing kinase activity Source: UniProtKB
Apoptotic process Source: UniProtKB-KW
Negative regulation of apoptotic process Source: UniProtKB
Positive regulation of NF-kappaB transcription factor activity Source: UniProtKB
Positive regulation of protein phosphorylation Source: UniProtKB
Tumor necrosis factor-mediated signaling pathway Source: UniProtKB
Cellular Location
Cytoplasm
Involvement in disease
Psoriasis 2 (PSORS2): 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.
Pityriasis rubra pilaris (PRP): A rare, papulosquamous skin disease characterized by the appearance of keratotic follicular papules, well-demarcated salmon-colored erythematous plaques covered with fine powdery scales interspersed with distinct islands of uninvolved skin, and palmoplantar keratoderma. Most cases are sporadic. The rare familial cases show autosomal dominant inheritance with incomplete penetrance and variable expression. Familial PRP usually presents at birth or appears during the first years of life and runs a chronic course. It is characterized by prominent follicular hyperkeratosis, diffuse palmoplantar keratoderma, and erythema.

Kelleni, M. (2021). NSAIDs, SARS CoV-2 ORF Proteins, Caspases, and CARD14: Solving the Mystery of COVID-19 and Beyond.

Van Nuffel, E., Staal, J., Baudelet, G., Haegman, M., Driege, Y., Hochepied, T., ... & Beyaert, R. (2020). MALT 1 targeting suppresses CARD 14‐induced psoriatic dermatitis in mice. EMBO reports, 21(7), e49237.

Mellett, M. (2020). Regulation and dysregulation of CARD14 signalling and its physiological consequences in inflammatory skin disease. Cellular Immunology, 354, 104147.

Peled, A., Sarig, O., Sun, G., Samuelov, L., Ma, C. A., Zhang, Y., ... & Sprecher, E. (2019). Loss-of-function mutations in caspase recruitment domain-containing protein 14 (CARD14) are associated with a severe variant of atopic dermatitis. Journal of Allergy and Clinical Immunology, 143(1), 173-181.

Zotti, T., Polvere, I., Voccola, S., & Vito, P. (2018). CARD14/CARMA2 signaling and its role in inflammatory skin disorders. Frontiers in immunology, 9, 2167.

Mellett, M., Meier, B., Mohanan, D., Schairer, R., Cheng, P., Satoh, T. K., ... & French, L. E. (2018). CARD14 gain-of-function mutation alone is sufficient to drive IL-23/IL-17–mediated psoriasiform skin inflammation in vivo. Journal of Investigative Dermatology, 138(9), 2010-2023.

Craiglow, B. G., Boyden, L. M., Hu, R., Virtanen, M., Su, J., Rodriguez, G., ... & Choate, K. A. (2018). CARD14-associated papulosquamous eruption: a spectrum including features of psoriasis and pityriasis rubra pilaris. Journal of the American Academy of Dermatology, 79(3), 487-494.

Lwin, S. M., Hsu, C. K., Liu, L., Huang, H. Y., Levell, N. J., & McGrath, J. A. (2018). Beneficial effect of ustekinumab in familial pityriasis rubra pilaris with a new missense mutation in CARD 14. British Journal of Dermatology, 178(4), 969-972.

Wang, M., Zhang, S., Zheng, G., Huang, J., Songyang, Z., Zhao, X., & Lin, X. (2018). Gain-of-function mutation of Card14 leads to spontaneous psoriasis-like skin inflammation through enhanced keratinocyte response to IL-17A. Immunity, 49(1), 66-79.

Israel, L., & Mellett, M. (2018). Clinical and genetic heterogeneity of CARD14 mutations in psoriatic skin disease. Frontiers in immunology, 9, 2239.

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For research use only. Not intended for any clinical use.

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