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Validated All-in-One™ qPCR Primer for CYLD(NM_015247.3) Search again
Product ID:
HQP152261
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
BRSS, CDMT, CYLD1, CYLDI, EAC, FTDALS8, MFT, MFT1, SBS, TEM, USPL2
Gene Description:
CYLD lysine 63 deubiquitinase
Target Gene Accession:
NM_015247.3(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Summary
This gene is encodes a cytoplasmic protein with three cytoskeletal-associated protein-glycine-conserved (CAP-GLY) domains that functions as a deubiquitinating enzyme. Mutations in this gene have been associated with cylindromatosis, multiple familial trichoepithelioma, and Brooke-Spiegler syndrome. Alternate transcriptional splice variants, encoding different isoforms, have been characterized. [provided by RefSeq].
Gene References into function
- CYLD is a deubiquitinating enzyme that negatively regulates activation of the transcription factor NF-kappaB by specific tumour-necrosis factor receptors (TNFRs)
- inhibition of cylindromatosis tumour suppressor gene (CYLD) enhances activation of NF-kappaB; inhibition of CYLD increases resistance to apoptosis, suggesting a mechanism through which loss of CYLD contributes to oncogenesis
- CYLD negatively regulates NF-kappaB signalling by deubiquitination; CYLD interacts with NEMO and TRAF2
- novel missense mutation in the CYLD gene, designated E474G in Brooke-Spiegler syndrome resembling trichoepithelioma
- CYLD interacts with TRIP and regulates negatively nuclear factor kappaB activation by tumor necrosis factor.
- CYLD is induced by NF-kappaB
- Mutations of the tumor suppressor gene CYLD at 16q12-q13 may give rise to familial trichoepithelioma indistinguishable from the phenotype assigned to 9p21.
- Data show that the third cytoskeleton-associated protein-glycine conserved domain of CYLD specifically interacts with one of the two proline-rich sequences of NEMO/IKKgamma.
- CYLD has a role in negative regulation of JNK signaling
- findings suggest that CYLD serves as a novel target of IKK and that the site-specific phosphorylation of CYLD regulates its signaling function
- The tumor suppressor familial cylindromatosis gene (CYLD) was found to be a direct target of BAF57 as determined by chromatin immunoprecipitation analysis. (CYLD)
- study provided direct evidence for the negative regulation of Toll-like receptor 2 (TLR2) signaling by the tumor suppressor cylindromatosis (CYLD)
- TRPA1 is a novel substrate for the de-ubiquitinating activity of CYLD, and this de-ubiquitination has the net effect of increasing the cellular pool of TRPA1 proteins.
- The combined delivery of CYLD and TRAIL may be a new useful strategy for hepatocellular carcinoma or other tumor cells with enhanced NF-kappaB activity.
- Mouse Cyld can negatively regulate different NF-kappaB pathways; inactivation of TRAF2 controls survival and inflammation, while inhibition of Bcl-3 controls proliferation and tumor growth.
- Reduced expression of CYLD is associated with colon and hepatocellular carcinomas
- additional function of CYLD could provide an explanation for the benign nature of most cylindroma lesions
- in cell line KM-H2, a 2.35 Mb deletion was found at 16q12.1 putatively defining a small critical region for the recurrent 16q deletion in Hodgkin's lymphoma. This region contains the CYLD gene, a known suppressor gene of the NF-mB pathway.
- identifies CYLD for the first time as a critical negative regulator of host antiviral response
- Gene mapping and expression analysis of 16q loss of heterozygosity identifies WWOX and CYLD as being important in determining clinical outcome in multiple myeloma.
- a heterozygous missense mutation c.1787 G > A (p.Gly596Asp, G596D) in CYLD exons was detected in a patient with multiple familial trichoepithelioma & affected family members; CYLD protein was not detected by staining in the trichoepithelioma tumour tissu
- D681 in CYLD is required for cleavage of K63-linked polyubiquitin chains
- study reports a novel CYLD gene mutation at nucleotide 2687 that carries out 1 amino acid change at glycine 896 in the 4 members of a family affected with trichoepithelioma but not in the proband
- CYLD acts as a negative regulator for NF-kappaB-dependent inflammation in vivo, hence protecting the host against detrimental inflammatory response to NTHi infection
- CYLD enhances tubulin polymerization into microtubules by lowering the critical concentration for microtubule assembly.
- the role of CYLD in the pathogenesis of skin appendage tumours characterised by cylindromas, trichoepitheliomas and/or spiradenomas.
- Report a novel missense mutation of CYLD gene in a Chinese family with multiple familial trichoepithelioma.
- Potential role of CYLD (Cylindromatosis) as a deubiquitinating enzyme in vascular cells.
- Results describe the crystal structure of the CYLD USP domain, revealing a distinctive architecture that provides molecular insights into its specificity toward Lys63-linked polyubiquitin.
- These studies bring new insights into the molecular pathogenesis of S. pneumoniae infections through the NFAT-dependent mechanism and further identify CYLD as a negative regulator for NFAT signaling.
- Loss of the UCH domain in CYLD may contribute to oncogenesis by enhancing the degradation of proteins that suppress cell proliferation or promote apoptosis.
- Loss of CYLD might be associated with development of salivary gland tumors
- Findings show that CYLD is a negative regulator of RIG-I-mediated innate antiviral response.
- The mutation in the present case is novel and is predicted to alter the canonical splice acceptor sequence, thereby preventing proper splicing of the transcript.