SAB4200061
Anti-CYLD (C-terminal) antibody produced in rabbit
~1.0 mg/mL, affinity isolated antibody
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Synonym(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
UNSPSC Code:
12352203
NACRES:
NA.41
Recommended Products
biological source
rabbit
Quality Level
conjugate
unconjugated
antibody form
affinity isolated antibody
antibody product type
primary antibodies
clone
polyclonal
form
buffered aqueous solution
mol wt
antigen ~110 kDa
species reactivity
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
UniProt accession no.
shipped in
dry ice
storage temp.
−20°C
target post-translational modification
unmodified
Gene Information
human ... CYLD(1540)
General description
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.
Biochem/physiol Actions
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.
Physical form
Solution in 0.01 M phosphate buffered saline, pH 7.4, containing 15 mM sodium azide.
Legal Information
ExtrAvidin is a registered trademark of Merck KGaA, Darmstadt, Germany
Disclaimer
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.
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Regulatory Information
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Certificates of Analysis (COA)
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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)
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)
Josefa P Alameda et al.
International journal of molecular sciences, 22(13) (2021-07-03)
Cylindromatosis (CYLD) is a deubiquitinase (DUB) enzyme that was initially characterized as a tumor suppressor of adnexal skin tumors in patients with CYLD syndrome. Later, it was also shown that the expression of functionally inactive mutated forms of CYLD promoted
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
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