IndraLab

Statements



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"Specific deletion of CYLD in Foxp3 Treg cells caused inflammation in the lungs correlating with their increased migratory activity into the lungs."

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"In addition, it is also possible that CYLD may inhibit ERK activation and inflammation via up-regulation of MAPK phosphatase-1 (MKP-1)."

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"CYLD also inhibited inflammation and proliferation in vascular cells and represented a novel target for the treatment or prevention of atherosclerosis [XREF_BIBR]."

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"NTHi induced CYLD, in turn, negatively regulates NTHi induced NF-kappaB activation through deubiquitinating TRAF6 and 7 and down-regulates inflammation."

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"Spontaneous lung inflammation caused by the CYLD cKO deficiency was also ameliorated by Scinderin deletion (Fig 6, F and G)."

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"As very recently described, the deubiquitinase Cyld regulates the function of the NLRP6 inflammasome and prevents excessive inflammation via the production of IL-18."

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"CYLD suppresses NF-kappaB-dependent inflammation by removing K63 linked polyubiquitin chains from TRAF2, TRAF6, NEMO, TAK1, Bcl3 and RIP1."

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"Since the majority of correlations were between IA genes and pro-inflammatory pathways and signatures, the dysregulation of CYLD represents an exception, and we hypothesize that CYLD may be expressed as a response to attenuate excessive inflammation."

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"Foxp3 restricted CYLD conditional knockout mice (cKO) were examined in mouse models of allergen induced airway inflammation and Nippostrongylus brasiliensis infection."

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"Similar results are seen in vivo; Cyld knockout mice, generated by Zhang et al. [21], were susceptible to induced colonic inflammation by using colitis associated cancer (CAC)."

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"In conclusion, these data demonstrate that the deubiquitinating enzyme CYLD may inhibit inflammation and proliferation in vascular cells and may represent a novel target for the treatment or prevention of atherosclerosis."

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"In line with the studies described above (134), CYLD knockout caused increased destruction of intestinal epithelia and severe colonic inflammation when challenged by pathological factors."

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"In a similar study, CYLD was shown to negatively regulate NF-kappaB activation and lung inflammation in mice infected with non typeable Haemophilus influenzae 22."

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"Methods:. Foxp3-restricted CYLD conditional knockout mice (cKO) were examined in mouse models of allergen-induced airway inflammation and Nippostrongylus brasiliensis infection."

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"Recent insights into the normal functions and signaling interactions of the CYLD gene product indicate that CYLD interferes with NF-kappaB, JNK, and p38MAPK signaling to limit inflammation and cancer,[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"Similarly , deficiency in CYLD or A20 , a master regulator of NFkappaB , lead to overt pathway activation and inflammation ( 132 ) ."

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"This is in contrast with dysregulated TNFR1 signaling commonly observed in liver disease and cancer and the fact that liver specific deletion of CYLD induces TNFR1 mediated liver inflammation and development of hepatocellular carcinoma [XREF_BIBR, XREF_BIBR]."

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"CYLD restricts inflammation by inhibiting NFkappaB activation [XREF_BIBR], yet it can induce innate immune responses by stabilizing STING, a cytosolic DNA sensor and a major regulator of type I interferon signaling, via its deubiquitination on K48 linked chains [XREF_BIBR]."
| PMC

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"For example, CYLD has been shown to downregulate the inflammatory response following bacterial infection with Escherichia coli by negatively regulating the innate immune response via inhibition of NF-kappaB signalling."

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"Reduced expression of CYLD promotes cell survival and inflammation in gefitinib treated NSCLC PC-9 cells : targeting CYLD may be beneficial for acquired resistance to gefitinib therapy."

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"Focusing on recent data concerning the normal functions and signaling interactions of the CYLD gene product, we explain how CYLD interferes with TNF-alpha or TLR mediated signaling as well as with JNK or NF-kappaB-dependent p65/50 signaling to limit inflammation."

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"Previous studies indicate that CYLD overexpression reduced inflammation during acute or chronic liver injury."

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"CYLD restricts inflammation by inhibiting NFkappaB activation [ 52 ] , yet it can induce innate immune responses by stabilizing STING , a cytosolic DNA sensor and a major regulator of type I interferon signaling , via its deubiquitination on K48-linked chains [ 53 ] ."
| PMC

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"Although additional studies are needed to clarify the molecular mechanisms, our in vitro data suggested that hypoxia induced CYLD reduction may promote inflammation in an autocrine and paracrine fashion in GBM tissues."

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"CYLD is an inhibitor of inflammation [53]."

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"As shown in XREF_FIG, PDE4B knockdown selectively inhibited activation of JNK2 but not JNK1, thereby confirming that PDE4B negatively regulates NTHi induced CYLD expression and mediates inflammation via specific activation of JNK2 but not JNK1."

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"These data indicate that, depending on the external signals, 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."

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"We also have shown that the deubiquitinase cylindromatosis (CYLD) suppresses NTHi induced inflammation."

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"In the present study, we identified PDE4B as a key negative regulator for CYLD via selective activation of c-jun N-terminal kinase 2 (JNK2), but not JNK1, and inhibition of PDE4B significantly enhanced NTHi induced CYLD expression and suppressed inflammation."

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"We will further pursue studies to determine if the DUB activity of CYLD is required for CYLD-mediated suppression of inflammatory response induced by S. pneumoniae."

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"We observed that overexpression of Cyld in hepatocytes concomitantly inhibits lipid accumulation, insulin resistance, inflammation and fibrosis in mice with NASH induced in an experimental setting."