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

Name: Mouse Anti-CARD14 Recombinant Antibody (CBXC-0067)
SKU: CBMAB-C5715-CQ
Rating: 5 (1 reviews)

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Datasheet

SDS

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Datasheet Target References Q & As Review & reward Protocols Associated Products

Basic Information

Host Animal

Mouse

Clone

CBXC-0067

Application

ELISA

Immunogen

CARD14 (905 a.a.-1004 a.a) partial recombinant protein with GST tag.

Host Species

Mouse

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

Preservative

None

Concentration

Batch dependent

Storage

Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freeze/thaw cycles.

More Infomation

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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Please try the standard protocols which include: protocols, troubleshooting and guide.

Enzyme-linked Immunosorbent Assay (ELISA)
Flow Cytometry
Immunofluorescence (IF)
Immunohistochemistry (IHC)
Immunoprecipitation (IP)
Western Blot (WB)
Enzyme-Linked Immunospot (ELISpot)
Proteogenomics
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