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SAB4200061

Sigma-Aldrich

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

~1.0 mg/mL, affinity isolated antibody

Synonyme(s) :

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

Code UNSPSC :
12352203
Nomenclature NACRES :
NA.41

Source biologique

rabbit

Niveau de qualité

200

Conjugué

unconjugated

Forme d'anticorps

affinity isolated antibody

Type de produit anticorps

primary antibodies

Clone

polyclonal

Forme

buffered aqueous solution

Poids mol.

antigen ~110 kDa

Espèces réactives

human

Concentration

~1.0 mg/mL

Technique(s)

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

Numéro d'accès UniProt

Q9NQC7

Conditions d'expédition

dry ice

Température de stockage

−20°C

Modification post-traductionnelle de la cible

unmodified

Informations sur le gène

human ... CYLD(1540)

Description générale

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.

Application

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

Actions biochimiques/physiologiques

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.

Forme physique

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

Informations légales

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

Clause de non-responsabilité

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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Code de la classe de stockage

10 - Combustible liquids

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable

Certificats d'analyse (COA)

Recherchez un Certificats d'analyse (COA) en saisissant le numéro de lot du produit. Les numéros de lot figurent sur l'étiquette du produit après les mots "Lot" ou "Batch".

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Consulter la Bibliothèque de documents

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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