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SAB4200061

Sigma-Aldrich

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

~1.0 mg/mL, affinity isolated antibody

Sinônimo(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

Código UNSPSC:
12352203
NACRES:
NA.41

fonte biológica

rabbit

conjugado

unconjugated

forma do anticorpo

affinity isolated antibody

tipo de produto de anticorpo

primary antibodies

clone

polyclonal

Formulário

buffered aqueous solution

peso molecular

antigen ~110 kDa

reatividade de espécies

human

concentração

~1.0 mg/mL

técnica(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

nº de adesão UniProt

Q9NQC7

Condições de expedição

dry ice

temperatura de armazenamento

−20°C

modificação pós-traducional do alvo

unmodified

Informações sobre genes

human ... CYLD(1540)

Categorias relacionadas

Descrição geral

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.

Aplicação

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

Ações bioquímicas/fisiológicas

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.

forma física

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

Informações legais

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

Exoneração de responsabilidade

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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Código de classe de armazenamento

10 - Combustible liquids

Ponto de fulgor (°F)

Not applicable

Ponto de fulgor (°C)

Not applicable

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Certificados de análise (COA)

Lot/Batch Number
119M4759V
21190833
010M4780

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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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