Product Description
Size: 100µg
Mouse Monoclonal CYLD antibody. N-terminal. Suitable for IHC-P, WB, ICC/IF and reacts with Mouse, Human samples. Cited in 2 publications. Immunogen corresponding to Recombinant Fragment Protein within Human CYLD.
Key facts
Host species:Mouse,
Clonality:Monoclonal,
Clone number:733,
Isotype:IgG1,
Carrier free:No,
Reacts with:Human, Mouse,
Applications:WB, ICC/IF, IHC-PSee reactivity dataSee the reactivity data table below for information on validated species and application combinations.,
Immunogen:Recombinant Fragment Protein within Human CYLD. The exact immunogen used to generate this antibody is proprietary information.Q9NQC7,
Specificity:The immunogen is 98% similar to bovine and 92% similar to rat sequences.
Properties and Storage Information:
Form-Liquid, Purification technique-Affinity purification Protein A, Storage buffer-pH: 7.4Preservative: 0.1% Sodium azideConstituents: PBS, Shipped at conditions-Blue Ice, Appropriate short-term storage duration-1-2 weeks, Appropriate short-term storage conditions-+4°C, Appropriate long-term storage conditions--20°C, Aliquoting information-Upon delivery aliquot, Storage information-Avoid freeze / thaw cycle
Supplementary Information:
This supplementary information is collated from multiple sources and compiled automatically.
CYLD also known as cylindromatosis or turban tumor syndrome is a protein that serves mainly as a deubiquitinating enzyme. This protein has a mass of approximately 108 kDa and is expressed in a variety of tissues most notably the skin and lungs. It is a negative regulator of cell signaling cascades particularly in pathways where ubiquitination needs to be controlled. CYLD interacts directly with other proteins to remove ubiquitin chains a process that is essential for regulating the degradation of proteins and maintaining cellular functions.
Biological function summary
The deubiquitination activity of CYLD plays a critical role in controlling inflammation and cell proliferation. This protein often associates with complexes that regulate the activity of NF-kB signaling pathways. By removing ubiquitin from specific substrates CYLD limits the activation of NF-kB therefore modulating inflammatory responses in the body. Additionally CYLD's role extends to controlling cell cycle progression and preventing uncontrolled cell growth making it essential in tissue homeostasis.
Pathways
CYLD is a significant regulator of the NF-kB and Wnt signaling pathways. It interacts with proteins such as TRAF2 TRAF6 and NEMO which are important in these pathways. CYLD prevents constitutive activation of NF-kB therefore serving as a checkpoint in inflammation and immune response. In the Wnt signaling pathway CYLD's regulation affects the turnover of beta-catenin highlighting its role in developmental processes and cellular differentiation.
CYLD is closely associated with cylindromatosis and familial adenomatous polyposis. Mutations or disruptions in CYLD function can lead to these conditions where abnormal cell proliferation occurs due to unregulated NF-kB activation. In cylindromatosis CYLD mutations result in the benign skin tumors known as cylindromas. Furthermore its connection to proteins like TRAF2 links it to other tumorigenic processes emphasizing CYLD's influence in both inflammatory and proliferative disorders.
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Collaboration
Tony Tang
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