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The crystal structures representing the catalytic states of zebrafish CYLD for Met1 (show DNMT1 ELISA Kits)- and Lys63-linked Ub chains and two distinct precatalytic states for Met1 (show DNMT1 ELISA Kits)-linked chains are presented.
Our findings underscore a critical tumor-suppressing role for functional intestinal epithelial CYLD in colitis-associated carcinogenesis
Deubiquitinase CYLD negatively regulates MyD88 (show MYD88 ELISA Kits)-mediated signaling by directly interacting with MyD88 (show MYD88 ELISA Kits) and deubiquitinating nontypeable Haemophilus influenzae (NTHi)-induced K63-linked polyubiquitination of MyD88 (show MYD88 ELISA Kits) at lysine 231.
CYLD interrupts the ERK (show EPHB2 ELISA Kits)- and p38 (show CRK ELISA Kits)-/AP-1 (show JUN ELISA Kits) and c-Myc (show MYC ELISA Kits) pathways to suppress Nrf2 (show NFE2L2 ELISA Kits)-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 (show NFASC ELISA Kits)-kappaB (show NFKB1 ELISA Kits) essential modulator (NEMO (show IKBKG ELISA Kits)) and cylindromatosis protein double mutant mice is mediated by TNF (show TNF ELISA Kits) receptor 1 (TNFR1 (show TNFRSF1A ELISA Kits)) signaling and can be rescued by TNFR1 (show TNFRSF1A ELISA Kits) deficiency.
CYLD is a central regulator of apoptotic cell death in murine hepatocytes by controlling NF-kappaB (show NFKB1 ELISA Kits) 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 (show UBB ELISA Kits) chain from centrosomal protein of 70 kDa (Cep70 (show CEP70 ELISA Kits)), a requirement for Cep70 (show CEP70 ELISA Kits) to interact with gamma-tubulin (show TUBG1 ELISA Kits) and localize at the centrosome.
CYLD negatively regulates nontypeable Haemophilus influenzae-induced IL-8 (show IL8 ELISA Kits) expression via MKP-1 (show DUSP1 ELISA Kits)-dependent inhibition of ERK (show EPHB2 ELISA Kits).
These results demonstrate the involvement of histone deacetylases in the down regulation of Cyld expression in hepatocellular carcinoma cells.
Novel CYLD germline mutations c.1821_1826+1delinsCT/L607Ffs*9, c.2666A>T/p.D889V and c.2712delT/p.905Kfs*8 were identified in unrelated Brooke-Spiegler Syndrome patients.
Study founds the levels of CYLD and SMAD7 (show SMAD7 ELISA Kits) significantly decreased in oral squamous cell carcinoma (OSSC) cells and proposes a model that CYLD suppresses OSCC metastases through SMAD7 (show SMAD7 ELISA Kits). Downregulation of CYLD appears to directly contribute to the distal metastases of primary OSCC and subsequently poor prognosis.
Haplotype analysis was performed for the patients with multiple familial trichoepithelioma type 1, patients with familial cylindromatosis and a patient with Brooke-Spiegler syndrome, all of whom carry the same heterozygous nonsense CYLD mutation.
Ultraviolet radiation induced CYLD translocation from the cytoplasm to microtubules, posttranslational modification and degradation in a proteasome-independent manner.
CYLD interrupts the ERK (show EPHB2 ELISA Kits)- and p38 (show CRK ELISA Kits)-/AP-1 (show FOSB ELISA Kits) and c-Myc (show MYC ELISA Kits) pathways to suppress Nrf2 (show GABPA ELISA Kits)-operated antioxidative capacity, thereby enhancing oxidative stress in the heart.
Data suggest OPTN (optineurin (show OPTN ELISA Kits)) is involved in up-regulation of innate immunity in mitosis; mechanism involves phosphorylation/nuclear translocation of CYLD and phosphorylation/mitochondrial translocation of TBK1 (NF-kB-activating kinase (show TBK1 ELISA Kits)).
CaMKII (show CAMK2G ELISA Kits)-mediated recruitment and upregulation of CYLD is expected to remove K63-linked polyubiquitins and facilitate proteasomal degradation at the postsynaptic density.
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.
cylindromatosis (turban tumor syndrome)
, probable ubiquitin carboxyl-terminal hydrolase CYLD-like
, ubiquitin carboxyl-terminal hydrolase CYLD
, deubiquitinating enzyme CYLD
, ubiquitin thioesterase CYLD
, ubiquitin thiolesterase CYLD
, ubiquitin-specific-processing protease CYLD
, probable ubiquitin carboxyl-terminal hydrolase CYLD
, retinitis pigmentosa 1 homolog
, ubiquitin specific peptidase like 2