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anti-Human CYLD Anticorps:
anti-Mouse (Murine) CYLD Anticorps:
anti-Rat (Rattus) CYLD Anticorps:
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Mouse (Murine) Polyclonal CYLD Primary Antibody pour ELISA, WB - ABIN188848
Massoumi, Chmielarska, Hennecke, Pfeifer, Fässler: Cyld inhibits tumor cell proliferation by blocking Bcl-3-dependent NF-kappaB signaling. dans Cell 2006
Polyclonal CYLD Primary Antibody pour WB - ABIN540750
Hellerbrand, Bumes, Bataille, Dietmaier, Massoumi, Bosserhoff: Reduced expression of CYLD in human colon and hepatocellular carcinomas. dans Carcinogenesis 2006
Human Polyclonal CYLD Primary Antibody pour ICC, IF - ABIN252428
Moranta, Regueiro, March, Llobet, Margareto, Larrarte, Larrate, Garmendia, Bengoechea: Klebsiella pneumoniae capsule polysaccharide impedes the expression of beta-defensins by airway epithelial cells. dans Infection and immunity 2010
Cow (Bovine) Polyclonal CYLD Primary Antibody pour ICC, IF - ABIN410065
Wu, Mu, Gao, Wang, Sy, Li: Prion protein is required for tumor necrosis factor α (TNFα)-triggered nuclear factor κB (NF-κB) signaling and cytokine production. dans The Journal of biological chemistry 2017
Our study revealed high incidence and sequential CYLD mutations in both basal cell adenoma and adenocarcinoma supporting a single neoplastic continuum for their evolution
Study reveals alterations of the CYLD gene in 15/15 cylindromas and 5/17 spiradenomas, yet only 2/24 spiradenocarcinomas. Also, a recurrent missense mutation found in the kinase domain of the ALPK1 gene in spiradenomas and spiradenocarcinomas, which is mutually exclusive from mutation of CYLD and can activate the NF-kappaB pathway in reporter assays.
miR-301b plays an oncogenic role in triple negative breast cancer (TNBC) possibly by downregulating CYLD and subsequently activating NF-kappaB p65, and this may provide a novel therapeutic approach for TNBC.
Study revealed that miR-182 expression was significantly upregulated in human gastrointestinal stromal tumors (GISTs) compared with adjacent normal tissues. Overexpression of miR-182 enhanced GIST-T1 cell growth, with increased proliferation and decreased apoptosis. In addition, cylindromatosis (CYLD) was identified as a direct target of miR-182.
A substantial number of CLL patient samples express sCYLD.
No genotype-phenotype correlation was found in tumor disorders of the skin appendages associated with mutations in the CYLD gene.
Catalytic domain mutation in CYLD gene is associated with osteosarcoma.
Studied the role of maternally expressed 3 (lncRNA-MEG3) as an antitumor lncRNA for malignant melanoma by regulating miR-499-5p/CYLD axis.
CYLD inhibits post-transcriptional regulation of RIG-I and MDA5 expression following TLR3 activation in MCs. CYLD may be involved in the pathogenesis of CKD
miR-197-3p-induced downregulation of CYLD promotes cell proliferation and inhibits cell apoptosis in lung adenocarcinoma cell lines.
Knockdown of CYLD expression reversed the cell proliferation promotion by miR1288in in glioblastoma.
TNF phase III signalling displays ongoing TNFR1/NF-kappa B activation in monocytic cells. High- and low-sensitive genes are induced including differentially regulated A20. A20 strictly controls this signalling in an IKK- and partially RIP-dependent manner. The A20-mediated control mechanisms are supported by ABIN1 and CYLD.
Low expression of CYLD is associated with glioma.
theses data show that CYLD regulates the magnitude of ubiquitination of several major effectors of the EGFR pathway by assisting the recruitment of the ubiquitin ligase Cbl-b to the activated EGFR complex.
Through deceasing the expression of Cylindromatosis (CYLD), a K63-specific DUB and endogenous blocker of NF-kappaB signaling, miR-130b can in return sustain the persistent activation of NF-kappaB, which may promote the malignant progression of transitional cell carcinoma of bladder.
While previous reports have described CYLD as a regulator of DVL proteins; this data suggests the presence of a more complicated reciprocal regulatory mechanism in CML cell lines.
Thrombin-mediated MALT1 protease activation triggers acute disruption of endothelial barrier integrity via CYLD cleavage.
MiR-767 acted as a role of tumor promoter by targeting CYLD in human melanoma.
SPATA2 has been described as a previously unrecognized factor in the linear ubiquitin chain assembly complex-dependent signaling pathways that serves as an adaptor between HOIP and CYLD, thereby enabling recruitment of CYLD to signaling complexes.
The data reveal SPATA2 as a high-affinity binding partner of CYLD and HOIP, and a regulatory component of linear ubiquitin chain assembly complex-mediated NF-kappaB signaling.
our findings demonstrate that CYLD mitigates Nonalcoholic steatohepatitis severity and identify the CYLD-TAK1 axis as a promising therapeutic target for management of the disease.
Loss of CYLD catalytic activity causes impaired DNA damage-induced p53 stabilization and activation in epithelial cells and sensitizes mice to chemical carcinogen-induced intestinal and skin tumorigenesis.
The present results support the involvement of CYLD in the regulation of NF-kappaB inflammatory signaling induced by elevated glucose, implicating CYLD as a potential therapeutic target of diabetic nephropathy .
the role of CYLD in development, tissue homeostasis, and tumorigenesis
Findings provide physiological insight into the ciliary role of the CYLD/HDAC6 axis and suggest a functional interplay between these two proteins in ciliary homeostasis.
TLR4 activates CASPASE-8 to cleave and remove the deubiquitinase cylindromatosis (CYLD) in a TRIF- and RIPK1-dependent manner to disable necroptosis in macrophages.
CYLD contributes to the transdifferentiation of adventitial fibroblasts via deubiquitinating Nox4 and may play a role in vascular remodeling.
this study shows that by polarization of the T cell cytokine response, CYLD can favor the development of allergic airway disease
Our findings underscore a critical tumor-suppressing role for functional intestinal epithelial CYLD in colitis-associated carcinogenesis
Deubiquitinase CYLD negatively regulates MyD88-mediated signaling by directly interacting with MyD88 and deubiquitinating nontypeable Haemophilus influenzae (NTHi)-induced K63-linked polyubiquitination of MyD88 at lysine 231.
CYLD interrupts the ERK- and p38-/AP-1 and c-Myc pathways to suppress Nrf2-operated antioxidative capacity, thereby enhancing oxidative stress in the heart.
Our data demonstrate that inefficient negative selection in the thymus of CYLD(ex7/8) mice result from a defect in mTEC maturation.
The deubiquitinating enzyme CYLD controls apical docking of basal bodies in ciliated epithelial cells.
Data show that the in utero death of NF-NF-kappaB essential modulator (NEMO) and cylindromatosis protein double mutant mice is mediated by TNF receptor 1 (TNFR1) signaling and can be rescued by TNFR1 deficiency.
CYLD is a central regulator of apoptotic cell death in murine hepatocytes by controlling NF-kappaB dependent anti-apoptotic signaling.
In contrast to full-length CYLD, the immune function of short splice variant CYLD (sCYLD) is insufficiently described. To explore sCYLD's function in infection, investigated whether dendritic cell-specific sCYLD regulates the pathogenesis of listeriosis.
The ciliary function of CYLD is partially attributed to its deconjugation of the polyubiquitin chain from centrosomal protein of 70 kDa (Cep70), a requirement for Cep70 to interact with gamma-tubulin and localize at the centrosome.
CYLD negatively regulates nontypeable Haemophilus influenzae-induced IL-8 expression via MKP-1-dependent inhibition of ERK.
The crystal structures representing the catalytic states of zebrafish CYLD for Met1- and Lys63-linked Ub chains and two distinct precatalytic states for Met1-linked chains are presented.
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.
deubiquitinating enzyme CYLD
, probable ubiquitin carboxyl-terminal hydrolase CYLD
, ubiquitin carboxyl-terminal hydrolase CYLD
, ubiquitin specific peptidase like 2
, ubiquitin thioesterase CYLD
, ubiquitin thiolesterase CYLD
, ubiquitin-specific-processing protease CYLD
, cylindromatosis (turban tumor syndrome)
, probable ubiquitin carboxyl-terminal hydrolase CYLD-like
, retinitis pigmentosa 1 homolog