Applied Filters:

Keyword:'18079'

Showing 1-30 of 407 results for "

18079

" within Papers

Drp1 stabilizes p53 on the mitochondria to trigger necrosis under oxidative stress conditions in vitro and in vivo.

Xing Guo et al.

The Biochemical journal, 461(1), 137-146 (2014-04-25)

Oxidative-stress-induced necrosis is considered to be one of the main pathological mediators in various neurological disorders, such as brain ischaemia. However, little is known about the mechanism by which cells modulate necrosis in response to oxidative stress. In the present

Clearance of PML/RARA-bound promoters suffice to initiate APL differentiation.

Adeline Vitaliano-Prunier et al.

Blood, 124(25), 3772-3780 (2014-09-27)

PML/RARA, a potent transcriptional inhibitor of nuclear receptor signaling, represses myeloid differentiation genes and drives acute promyelocytic leukemia (APL). Association of the retinoid X receptor-α (RXRA) coreceptor to PML/RARA is required for transformation, with RXRA promoting its efficient DNA binding.

Targeting protein neddylation with an NEDD8-activating enzyme inhibitor MLN4924 induced apoptosis or senescence in human lymphoma cells.

Yanchun Wang et al.

Cancer biology & therapy, 16(3), 420-429 (2015-03-18)

Recent studies indicate that post-translational protein neddylation is required for the maintenance of cell viability in several lymphoma cell lines, while inhibition of the neddylation pathway with an NEDD8-activating enzyme (NAE) inhibitor MLN4924 induces apoptosis in lymphoma cells. However, the

SKP2 inactivation suppresses prostate tumorigenesis by mediating JARID1B ubiquitination.

Wenfu Lu et al.

Oncotarget, 6(2), 771-788 (2015-01-19)

Aberrant elevation of JARID1B and histone H3 lysine 4 trimethylation (H3K4me3) is frequently observed in many diseases including prostate cancer (PCa), yet the mechanisms on the regulation of JARID1B and H3K4me3 through epigenetic alterations still remain poorly understood. Here we

Viral suppressors of the RIG-I-mediated interferon response are pre-packaged in influenza virions.

Swantje Liedmann et al.

Nature communications, 5, 5645-5645 (2014-12-10)

The type I interferon (IFN) response represents the first line of defence to invading pathogens. Internalized viral ribonucleoproteins (vRNPs) of negative-strand RNA viruses induce an early IFN response by interacting with retinoic acid inducible gene I (RIG-I) and its recruitment

Influenza A virus-induced degradation of eukaryotic translation initiation factor 4B contributes to viral replication by suppressing IFITM3 protein expression.

Song Wang et al.

Journal of virology, 88(15), 8375-8385 (2014-05-16)

Although alteration in host cellular translation machinery occurs in virus-infected cells, the role of such alteration and the precise pathogenic processes are not well understood. Influenza A virus (IAV) infection shuts off host cell gene expression at transcriptional and translational

A novel firefly luciferase biosensor enhances the detection of apoptosis induced by ESAT-6 family proteins of Mycobacterium tuberculosis.

Junwei Shi et al.

Biochemical and biophysical research communications, 452(4), 1046-1053 (2014-09-23)

The activation of caspase-3 is a key surrogate marker for detecting apoptosis. To quantitate caspase-3 activity, we constructed a biosensor comprising a recombinant firefly luciferase containing a caspase-3 cleavage site. When apoptosis was induced, caspase-3 cleavage of the biosensor activated

Association of the in vitro susceptibility of clinical isolates of chlamydia trachomatis with serovar and duration of antibiotic exposure.

Heping Zheng et al.

Sexually transmitted diseases, 42(3), 115-119 (2015-02-11)

The presence of persistent Chlamydia trachomatis infection after treatment does not always correlate with in vitro susceptibility testing. The in vitro minimum inhibitory concentration (MIC) and minimal bactericidal concentration (MBC) of azithromycin, clarithromycin, roxithromycin, doxycycline, tetracycline, ofloxacin, and penicillin were

Molecular basis for premature senescence induced by surfactants in normal human cells.

Yoshimi Yamakami et al.

Bioscience, biotechnology, and biochemistry, 78(12), 2022-2029 (2014-09-10)

Sublethal doses of surfactants as exemplified by NP-40 clearly induce premature senescence in normal human cells. To understand molecular basis for this phenomenon, we tried to suppress it with use of various inhibitors. An inhibitor of p38 of the MAPK

Rer1 and calnexin regulate endoplasmic reticulum retention of a peripheral myelin protein 22 mutant that causes type 1A Charcot-Marie-Tooth disease.

Taichi Hara et al.

Scientific reports, 4, 6992-6992 (2014-11-12)

Peripheral myelin protein 22 (PMP22) resides in the plasma membrane and is required for myelin formation in the peripheral nervous system. Many PMP22 mutants accumulate in excess in the endoplasmic reticulum (ER) and lead to the inherited neuropathies of Charcot-Marie-Tooth

Regulation of Mdm2 protein stability and the p53 response by NEDD4-1 E3 ligase.

C Xu et al.

Oncogene, 34(3), 281-289 (2014-01-15)

Mdm2 is a critical negative regulator of the tumor suppressor protein p53. Mdm2 is an E3 ligase whose overexpression leads to functional inactivation of p53. Mdm2 protein stability is regulated by several mechanisms including RING (Really Interesting New Gene) domain-mediated

Cytokeratin19 induced by HER2/ERK binds and stabilizes HER2 on cell membranes.

J-h Ju et al.

Cell death and differentiation, 22(4), 665-676 (2014-10-25)

Cytokeratin19 (KRT19) is widely used as a biomarker for the detection of disseminated tumors. Using an LC-MS/MS proteomics approach, we found that KRT19 was upregulated in HER2-overexpressing cells and tissues. KRT19 expression was induced by HER2-downstream ERK at the transcriptional

XI-011 enhances cisplatin-induced apoptosis by functional restoration of p53 in head and neck cancer.

Jong-Lyel Roh et al.

Apoptosis : an international journal on programmed cell death, 19(11), 1594-1602 (2014-08-13)

Head and neck cancer (HNC), one of the most common cancers worldwide, frequently involves mutation of the TP53 gene and dysregulation of the p53 pathway. Overexpression of MDM2 or MDM4 inactivates the tumor-suppressive function of p53. Restoration of p53 function

Circovirus transport proceeds via direct interaction of the cytoplasmic dynein IC1 subunit with the viral capsid protein.

Jingjing Cao et al.

Journal of virology, 89(5), 2777-2791 (2014-12-30)

Microtubule transport of circovirus from the periphery of the cell to the nucleus is essential for viral replication in early infection. How the microtubule is recruited to the viral cargo remains unclear. In this study, we observed that circovirus trafficking

Mutations in potassium channel kcnd3 cause spinocerebellar ataxia type 19.

Anna Duarri et al.

Annals of neurology, 72(6), 870-880 (2013-01-03)

To identify the causative gene for the neurodegenerative disorder spinocerebellar ataxia type 19 (SCA19) located on chromosomal region 1p21-q21. Exome sequencing was used to identify the causal mutation in a large SCA19 family. We then screened 230 ataxia families for

Lyn tyrosine kinase regulates androgen receptor expression and activity in castrate-resistant prostate cancer.

A Zardan et al.

Oncogenesis, 3, e115-e115 (2014-08-19)

Castrate-resistant prostate cancer (CRPC) progression is a complex process by which prostate cells acquire the ability to survive and proliferate in the absence or under very low levels of androgens. Most CRPC tumors continue to express the androgen receptor (AR)

Hypoxia promotes stem cell phenotypes and poor prognosis through epigenetic regulation of DICER.

Twan van den Beucken et al.

Nature communications, 5, 5203-5203 (2014-10-30)

MicroRNAs are small regulatory RNAs that post transcriptionally control gene expression. Reduced expression of DICER, the enzyme involved in microRNA processing, is frequently observed in cancer and is associated with poor clinical outcome in various malignancies. Yet, the underlying mechanisms

Inhibition of ERK1/2 down-regulates the Hippo/YAP signaling pathway in human NSCLC cells.

Bin You et al.

Oncotarget, 6(6), 4357-4368 (2015-03-05)

Alterations of the EGFR/ERK and Hippo/YAP pathway have been found in non-small cell lung cancer (NSCLC). Herein, we show that ERK1 and ERK2 have an effect on the Hippo/YAP pathway in human NSCLC cells. Firstly, inhibition of ERK1/2 by siRNA

A survey of the interactome of Kaposi's sarcoma-associated herpesvirus ORF45 revealed its binding to viral ORF33 and cellular USP7, resulting in stabilization of ORF33 that is required for production of progeny viruses.

Joseph Gillen et al.

Journal of virology, 89(9), 4918-4931 (2015-02-20)

The ORF45 protein of Kaposi's sarcoma-associated herpesvirus (KSHV) is a gammaherpesvirus-specific immediate-early tegument protein. Our previous studies have revealed its crucial roles in both early and late stages of KSHV infection. In this study, we surveyed the interactome of ORF45

Regulation of cytokine-inducible SH2-containing protein (CIS) by ubiquitination and Elongin B/C interaction.

Philip J Jensik et al.

Molecular and cellular endocrinology, 401, 130-141 (2014-12-03)

Cytokine-inducible SH2-containing protein (CIS) inhibits prolactin receptor (PRLR) signaling and acts as part of an E3 ubiquitin ligase complex through interactions with Elongin B/C proteins. This study aimed to identify CIS lysine ubiquitination sites and determine roles of ubiquitination and

LIF negatively regulates tumour-suppressor p53 through Stat3/ID1/MDM2 in colorectal cancers.

Haiyang Yu et al.

Nature communications, 5, 5218-5218 (2014-10-18)

Leukaemia inhibitory factor (LIF) has been recently identified as a p53 target gene, which mediates the role of p53 in maternal implantation under normal physiological conditions. Here we report that LIF is a negative regulator of p53; LIF downregulates p53

The Type II Hsp40 Sis1 cooperates with Hsp70 and the E3 ligase Ubr1 to promote degradation of terminally misfolded cytosolic protein.

Daniel W Summers et al.

PloS one, 8(1), e52099-e52099 (2013-01-24)

Mechanisms for cooperation between the cytosolic Hsp70 system and the ubiquitin proteasome system during protein triage are not clear. Herein, we identify new mechanisms for selection of misfolded cytosolic proteins for degradation via defining functional interactions between specific cytosolic Hsp70/Hsp40

Microbiota and metabolites of aged bottled gueuze beers converge to the same composition.

Freek Spitaels et al.

Food microbiology, 47, 1-11 (2015-01-15)

Gueuze beers are prepared by mixing young and old lambic beers and are bottle-refermented spontaneously for aging. The present study analyzed the microbiota and metabolites present in gueuze beers that were aged between a few months and up to 17

Non-genotoxic activation of p53 through the RPL11-dependent ribosomal stress pathway.

Lucia Morgado-Palacin et al.

Carcinogenesis, 35(12), 2822-2830 (2014-10-27)

Nucleolar disruption has recently emerged as a relevant means to activate p53 through inhibition of HDM2 by ribosome-free RPL11. Most drugs that induce nucleolar disruption also possess important genotoxic activity, which can have lasting mutagenic effects. Therefore, it is of

Amyotrophic lateral sclerosis-linked mutant VAPB inclusions do not interfere with protein degradation pathways or intracellular transport in a cultured cell model.

Paola Genevini et al.

PloS one, 9(11), e113416-e113416 (2014-11-20)

VAPB is a ubiquitously expressed, ER-resident adaptor protein involved in interorganellar lipid exchange, membrane contact site formation, and membrane trafficking. Its mutant form, P56S-VAPB, which has been linked to a dominantly inherited form of Amyotrophic Lateral Sclerosis (ALS8), generates intracellular

Fragile X-like behaviors and abnormal cortical dendritic spines in cytoplasmic FMR1-interacting protein 2-mutant mice.

Kihoon Han et al.

Human molecular genetics, 24(7), 1813-1823 (2014-11-30)

Silencing of fragile X mental retardation 1 (FMR1) gene and loss of fragile X mental retardation protein (FMRP) cause fragile X syndrome (FXS), a genetic disorder characterized by intellectual disability and autistic behaviors. FMRP is an mRNA-binding protein regulating neuronal

Regulation of 53BP1 protein stability by RNF8 and RNF168 is important for efficient DNA double-strand break repair.

Yiheng Hu et al.

PloS one, 9(10), e110522-e110522 (2014-10-23)

53BP1 regulates DNA double-strand break (DSB) repair. In functional assays for specific DSB repair pathways, we found that 53BP1 was important in the conservative non-homologous end-joining (C-NHEJ) pathway, and this activity was dependent upon RNF8 and RNF168. We observed that

Molecular Characterization of a Novel Putative Partitivirus Infecting Cytospora sacchari, a Plant Pathogenic Fungus.

Mahtab Peyambari et al.

The plant pathology journal, 30(2), 151-158 (2014-10-08)

Three double-stranded RNAs (dsRNAs), approximately 1.85, 1.65 and 1.27 kb in size, were detected in an isolate of Cytospora sacchari from Iran. Partial nucleotide sequence revealed a 1,284 bp segment containing one ORF that potentially encodes a 405 aa protein.

Interaction with cyclin H/cyclin-dependent kinase 7 (CCNH/CDK7) stabilizes C-terminal binding protein 2 (CtBP2) and promotes cancer cell migration.

Yuchan Wang et al.

The Journal of biological chemistry, 288(13), 9028-9034 (2013-02-09)

CtBP2 has been demonstrated to possess tumor-promoting capacities by virtue of up-regulating epithelial-mesenchymal transition (EMT) and down-regulating apoptosis in cancer cells. As a result, cellular CtBP2 levels are considered a key factor determining the outcome of oncogenic transformation. How pro-tumorigenic

Deciphering the modulation of gene expression by type I and II interferons combining 4sU-tagging, translational arrest and in silico promoter analysis.

Mirko Trilling et al.

Nucleic acids research, 41(17), 8107-8125 (2013-07-09)

Interferons (IFN) play a pivotal role in innate immunity, orchestrating a cell-intrinsic anti-pathogenic state and stimulating adaptive immune responses. The complex interplay between the primary response to IFNs and its modulation by positive and negative feedback loops is incompletely understood.

Page 1 of 14