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Key Documents

SAB4200061

Sigma-Aldrich

Anti-CYLD (C-terminal) antibody produced in rabbit

~1.0 mg/mL, affinity isolated antibody

Sinonimo/i:

Anti-Cylindromatosis (turban tumor syndrome), deubiquitinating enzyme CYLD, Anti-Ubiquitin carboxyl-terminal hydrolase CYLD, Anti-Ubiquitin specific peptidase like 2, Anti-Ubiquitin thiolesterase CYLD

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About This Item

Codice UNSPSC:
12352203
NACRES:
NA.41

Origine biologica

rabbit

Livello qualitativo

Coniugato

unconjugated

Forma dell’anticorpo

affinity isolated antibody

Tipo di anticorpo

primary antibodies

Clone

polyclonal

Forma fisica

buffered aqueous solution

PM

antigen ~110 kDa

Reattività contro le specie

human

Concentrazione

~1.0 mg/mL

tecniche

immunohistochemistry: 10-20 μg/mL using biotin / ExtrAvidin®-Peroxidase staining of heat-retrieved formalin-fixed, paraffin-embedded human skin sections
western blot: 2.5-5.0 μg/mL using whole extract of HEK-293T cells overexpressing human CYLD

N° accesso UniProt

Condizioni di spedizione

dry ice

Temperatura di conservazione

−20°C

modifica post-traduzionali bersaglio

unmodified

Informazioni sul gene

human ... CYLD(1540)

Categorie correlate

Descrizione generale

CYLD is a tumor suppressor protein exhibiting deubiquitination enzyme (DUB) activity, that specifically cleaves Lys63 -linked polyUb. CYLD contains a ubiquitin C-terminal hydrolase (UCH) domain, which is responsible for the removal of ubiquitin chains, and three cytoskeleton-associated protein-glycine conserved (CAP-Gly) domains, which are found in various microtubule-binding proteins.

Applicazioni

Anti-CYLD (C-terminal) antibody produced in rabbit has been used immunoblotting and immunohistochemistry.

Azioni biochim/fisiol

CYLD physically interacts with many different proteins, some of which positively mediate signaling through the NF-κB and c-Jun N-terminal kinase (JNK) pathways and induces their deubiquitination. It controls cell proliferation, cell survival and inflammatory responses by negatively regulating NF-κB and/or JNK-signaling pathways. CYLD also regulates other physiological pathways such as cell cycle progression, spermatogenesis, and osteoclastogenesis. Mutations in the CYLD gene have been associated with cylindromatosis, multiple familial trichoepithelioma, and Brooke-Spiegler syndrome.

Stato fisico

Solution in 0.01 M phos­phate buffered saline, pH 7.4, containing 15 mM sodium azide.

Note legali

ExtrAvidin is a registered trademark of Merck KGaA, Darmstadt, Germany

Esclusione di responsabilità

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

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Codice della classe di stoccaggio

10 - Combustible liquids

Punto d’infiammabilità (°F)

Not applicable

Punto d’infiammabilità (°C)

Not applicable


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The tumour suppressor CYLD negatively regulates NF-kappaB signalling by deubiquitination
Kovalenko A, et al.
Nature, 424(6950), 801-801 (2003)
Premature aging and cancer development in transgenic mice lacking functional CYLD
Alameda JP, et al.
Aging (Albany. NY.), 11(1), 127-127 (2019)
Mehdi Baratchian et al.
The Journal of biological chemistry, 291(14), 7608-7620 (2016-02-13)
The viral FLICE-like inhibitory protein (FLIP) protein from Kaposi sarcoma-associated herpesvirus activates the NF-κB pathway by forming a stable complex with a central region (amino acids 150-272) of the inhibitor of NF-κB kinase (IKK) γ subunits, thereby activating IKK. Cellular
Mutations in the CYLD gene in Brooke-Spiegler syndrome, familial cylindromatosis, and multiple familial trichoepithelioma: lack of genotype-phenotype correlation
Bowen S, et al.
The Journal of Investigative Dermatology, 124(5), 919-920 (2005)
G R Bignell et al.
Nature genetics, 25(2), 160-165 (2000-06-03)
Familial cylindromatosis is an autosomal dominant genetic predisposition to multiple tumours of the skin appendages. The susceptibility gene (CYLD) has previously been localized to chromosome 16q and has the genetic attributes of a tumour-suppressor gene (recessive oncogene). Here we have

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