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https://www.readbyqxmd.com/read/28521627/disseminated-bacillus-calmette-gu%C3%A3-rin-osteomyelitis-in-twin-sisters-related-to-stat1-gene-deficiency
#1
Sabah Boudjemaa, Linda Dainese, Sébastien Héritier, Caroline Masserot, Samia Hachemane, Jean-Laurent Casanova, Aurore Coulomb, Jacinta Bustamante
Mendelian susceptibility to mycobacterial disease is a rare syndrome characterized by severe clinical infections usually caused by weakly virulent mycobacterial species such as Bacillus Calmette-Guérin vaccines and environmental nontuberculous mycobacteria or more virulent mycobacteria as mycobacterium tuberculosis. Since 1996, 9 genes including 7 autosomal ( STAT1, IFNGR1, IFNGR2, IL12B, IL12RB1, ISG15, and IRF8) and 2 X-linked genes ( NEMO and CYBB) have been identified. Allelic heterogeneity leaded to recognize about 18 genetic diseases with variable clinical phenotypes, but sharing a same physiological mechanism represented by a defect in human IL-12-dependant-INF-γ-mediated immunity...
June 2017: Pediatric and Developmental Pathology
https://www.readbyqxmd.com/read/28518071/nerve-sparing-mid-urethral-obstruction-nemo-in-female-small-rodents
#2
Martin Sidler, Karen J Aitken, Jia Xin Jiang, Darius J Bägli
Partial bladder outlet obstruction (pBOO) has a high prevalence, causes significant patient burden, and immense health care costs. The most common animal model to investigate bladder remodeling in pBOO are female rodents undergoing partial obstruction at the proximal urethra. Variability in the degree of obstruction and animal mortality are major concerns with proximal obstruction. Furthermore, dissecting around the proximal urethra and bladder neck jeopardizes bladder innervation. We developed a nerve-sparing mid-urethral obstruction (NeMO) model for pBOO avoiding the disadvantages of the traditional model...
April 25, 2017: Journal of Visualized Experiments: JoVE
https://www.readbyqxmd.com/read/28515292/molluscum-contagiosum-virus-mc159-abrogates-ciap1-nemo-interactions-and-inhibits-nemo-polyubiquitination
#3
Sunetra Biswas, Joanna L Shisler
Molluscum contagiosum virus (MCV) is a dermatotropic poxvirus that causes benign skin lesions. MCV lesions persist because of virally-encoded immune evasion molecules that inhibit anti-viral responses. The MCV MC159 protein suppresses NF-κB activation, a powerful anti-viral response, via interactions with the NEMO subunit of the IKK complex. Binding of MC159 to NEMO does not disrupt the IKK complex, implying that MC159 prevents IKK activation via an as-yet-identified strategy. Here, we demonstrated that MC159 inhibited NEMO polyubiquitination, a post-translational modification required for IKK and downstream NF-κB activation...
May 17, 2017: Journal of Virology
https://www.readbyqxmd.com/read/28515148/nemo-a-transcriptional-target-of-estrogen-and-progesterone-is-linked-to-tumor-suppressor-pml-in-breast-cancer
#4
Kelli E Valdez, Hanan S Elsarraj, Yan Hong, Sandra L Grimm, Lawrence R Ricci, Fang Fan, Ossama Tawfik, Lisa May, Therese Cusick, Marc Inciardi, Mark Redick, Jason Gatewood, Onalisa Winblad, Susan G Hilsenbeck, Dean P Edwards, Christy Hagan, Andrew K Godwin, Carol J Fabian, Fariba Behbod
The beneficial versus detrimental roles of estrogen plus progesterone (E+P) in breast cancer remains controversial. Here we report a beneficial mechanism of E+P treatment in breast cancer cells driven by transcriptional upregulation of the NFκB modulator NEMO, which in turn promotes expression of the tumor suppressor protein PML. E+P treatment of patient-derived epithelial cells derived from ductal carcinoma in situ (DCIS) increased secretion of the pro-inflammatory cytokine IL-6. Mechanistic investigations indicated that IL-6 upregulation occurred as a result of transcriptional upregulation of NEMO, the gene for which harbored estrogen receptor (ER) binding sites within its promoter...
May 17, 2017: Cancer Research
https://www.readbyqxmd.com/read/28513998/ibd-due-to-pid-inflammatory-bowel-disease-caused-by-primary-immunodeficiencies-clinical-presentations-review-of-literature-and-proposal-of-a-rational-diagnostic-algorithm
#5
REVIEW
Daniel Tegtmeyer, Maximilian Seidl, Patrick Gerner, Ulrich Baumann, Christian Klemann
Inflammatory bowel diseases (IBD) including Crohn's disease (CD) and ulcerative colitis (UC) have a multifactorial pathogenesis with complex interactions between polygenetic predispositions and environmental factors. However, IBD can also be caused by monogenic diseases, such as primary immunodeficiencies (PID). Recently, an increasing number of these altogether rare diseases has been described to present often primarily, or solely as IBD. Early recognition of these conditions enables adaption of therapies and thus directly benefits the course of IBDs...
May 17, 2017: Pediatric Allergy and Immunology
https://www.readbyqxmd.com/read/28512628/dysplasia-of-granulocytes-in-a-patient-with-hpv-disease-recurrent-infections-and-b-lymphopenia-a-novel-variant-of-whim-syndrome
#6
Giusella M F Moscato, Erica Giacobbi, Lucia Anemona, Silvia Di Cesare, Gigliola Di Matteo, Massimo Andreoni, Alessandro Mauriello, Viviana Moschese
WHIM syndrome is a condition in which affected persons have chronic peripheral neutropenia, lymphopenia, abnormal susceptibility to human papilloma virus infection, and myelokathexis. Myelokathexis refers to the retention of mature neutrophils in the bone marrow (BM), which accounts for degenerative changes and hypersegmentation. Most patients present heterozygous autosomal dominant mutations of the gene encoding CXCR4. Consequently, aberrant CXCL12/CXCR4 signaling impairs the receptor downregulation causing hyperactivation (gain-of-function) that affects BM homing for myelopoiesis and lymphopoiesis and the release of neutrophils in the bloodstream...
2017: Frontiers in Pediatrics
https://www.readbyqxmd.com/read/28502111/asap3-upregulation-contributes-to-colorectal-carcinogenesis-and-indicates-poor-survival-outcome
#7
Haiying Tian, Jin Qian, Luoyan Ai, Yueyuan Li, Wenyu Su, Xian-Ming Kong, Jie Xu, Jing-Yuan Fang
The function and clinical implication of ArfGAP With SH3 Domain, Ankyrin Repeat And PH Domain 3 (ASAP3) in colorectal cancer (CRC) remains undefined. In the present study, we showed that the expression level of ASAP3 was dramatically increased in CRC and its upregulation was associated with American Joint Committee on Cancer (AJCC) stage (P<0.001) and poor prognosis (P=0.0022). The combination of AJCC stage and ASAP3 expression improved the prediction of survival in CRC patients. Suppression of ASAP3 inhibited cell proliferation by inducing G1-phase arrest without influencing apoptosis...
May 14, 2017: Cancer Science
https://www.readbyqxmd.com/read/28501618/assessing-activity-of-hepatitis-a-virus-3c-protease-using-a-cyclized-luciferase-based-biosensor
#8
Junwei Zhou, Dang Wang, Yongqiang Xi, Xinyu Zhu, Yuting Yang, Mengting Lv, Chuanzhen Luo, Jiyao Chen, Xu Ye, Liurong Fang, Shaobo Xiao
Hepatitis A is an acute infection caused by Hepatitis A virus (HAV), which is widely distributed throughout the world. The HAV 3C cysteine protease (3C(pro)), an important nonstructural protein, is responsible for most cleavage within the viral polyprotein and is critical for the processes of viral replication. Our group has previously demonstrated that HAV 3C(pro) cleaves human NF-κB essential modulator (NEMO), a kinase required in interferon signaling. Based on this finding, we generated four luciferase-based biosensors containing the NEMO sequence (PVLKAQ↓ADIYKA) that is cleaved by HAV 3C(pro) and/or the Nostoc punctiforme DnaE intein, to monitor the activity of HAV 3C(pro) in human embryonic kidney cells (HEK-293T)...
May 10, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/28490597/molluscum-contagiosum-virus-protein-mc005-inhibits-nf%C3%AE%C2%BAb-activation-by-targeting-nemo-regulated-ikk-activation
#9
Gareth Brady, Darya A Haas, Paul J Farrell, Andreas Pichlmair, Andrew G Bowie
Molluscum Contagiosum Virus (MCV), the only known extant, human-adapted poxvirus, causes a long-duration infection characterized by skin lesions that typically display an absence of inflammation despite containing high titres of live virus. Despite this curious presentation, MCV is very poorly characterized in terms of host-pathogen interactions. The absence of inflammation around MCV lesions suggests the presence of potent inhibitors of human anti-viral immunity and inflammation. However, only a small number of MCV immunomodulatory genes have been characterized in detail...
May 10, 2017: Journal of Virology
https://www.readbyqxmd.com/read/28481361/linear-ubiquitination-of-cytosolic-salmonella-typhimurium-activates-nf-%C3%AE%C2%BAb-and-restricts-bacterial-proliferation
#10
Sjoerd J L van Wijk, Franziska Fricke, Lina Herhaus, Jalaj Gupta, Katharina Hötte, Francesco Pampaloni, Paolo Grumati, Manuel Kaulich, Yu-Shin Sou, Masaaki Komatsu, Florian R Greten, Simone Fulda, Mike Heilemann, Ivan Dikic
Ubiquitination of invading Salmonella Typhimurium triggers autophagy of cytosolic bacteria and restricts their spread in epithelial cells. Ubiquitin (Ub) chains recruit autophagy receptors such as p62/SQSTM1, NDP52/CALCOCO and optineurin (OPTN), which initiate the formation of double-membrane autophagosomal structures and lysosomal destruction in a process known as xenophagy. Besides this, the functional consequences and mechanistic regulation of differentially linked Ub chains at the host-Salmonella interface have remained unexplored...
May 8, 2017: Nature Microbiology
https://www.readbyqxmd.com/read/28481331/lubac-synthesized-linear-ubiquitin-chains-restrict-cytosol-invading-bacteria-by-activating-autophagy-and-nf-%C3%AE%C2%BAb
#11
Jessica Noad, Alexander von der Malsburg, Claudio Pathe, Martin A Michel, David Komander, Felix Randow
Cell-autonomous immunity relies on the ubiquitin coat surrounding cytosol-invading bacteria functioning as an 'eat-me' signal for xenophagy. The origin, composition and precise mode of action of the ubiquitin coat remain incompletely understood. Here, by studying Salmonella Typhimurium, we show that the E3 ligase LUBAC generates linear (M1-linked) polyubiquitin patches in the ubiquitin coat, which serve as antibacterial and pro-inflammatory signalling platforms. LUBAC is recruited via its subunit HOIP to bacterial surfaces that are no longer shielded by host membranes and are already displaying ubiquitin, suggesting that LUBAC amplifies and refashions the ubiquitin coat...
May 8, 2017: Nature Microbiology
https://www.readbyqxmd.com/read/28479328/clinical-characteristics-of-patients-with-low-functional-il-6-production-upon-tlr-il-1r-stimulation
#12
Glynis Frans, Jutte Van der Werff Ten Bosch, Leen Moens, Greet Wuyts, Heidi Schaballie, David Tuerlinckx, Mia De Bie, Francois Vermeulen, Rik Schrijvers, Wim Meert, Matthew S Hestand, Joris Delanghe, Joris R Vermeesch, Isabelle Meyts, Xavier Bossuyt
Low IL-6 production upon stimulation by TLR/IL-1R ligands is associated with increased susceptibility to bacterial skin infections and to invasive infections with P. aeruginosa and/or with a IRAK-4/MyD88/NEMO defect.
May 4, 2017: Journal of Allergy and Clinical Immunology
https://www.readbyqxmd.com/read/28475177/the-role-of-hybrid-ubiquitin-chains-in-the-myd88-and-other-innate-immune-signalling-pathways
#13
REVIEW
Philip Cohen, Sam Strickson
The adaptor protein MyD88 is required for signal transmission by toll-like receptors and receptors of the interleukin-1 family of cytokines. MyD88 signalling triggers the formation of Lys63-linked and Met1-linked ubiquitin (K63-Ub, M1-Ub) chains within minutes. The K63-Ub chains, which are formed by the E3 ubiquitin ligases TRAF6, Pellino1 and Pellino2, activate TAK1, the master kinase that switches on mitogen-activated protein (MAP) kinase cascades and initiates activation of the canonical IκB kinase (IKK) complex...
May 5, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28469620/nf-%C3%AE%C2%BAb-pathway-in-autoinflammatory-diseases-dysregulation-of-protein-modifications-by-ubiquitin-defines-a-new-category-of-autoinflammatory-diseases
#14
REVIEW
Ivona Aksentijevich, Qing Zhou
Autoinflammatory diseases are caused by defects in genes that regulate the innate immunity. Recently, the scope of autoinflammation has been broadened to include diseases that result from dysregulations in protein modifications by the highly conserved ubiquitin (Ub) peptides. Thus far these diseases consist of linear ubiquitin chain assembly complex (LUBAC) and OTULIN deficiencies, and haploinsufficiency of A20. The LUBAC is critical for linear ubiquitination of key signaling molecules in immune response pathways, while deubiquitinase enzymes, OTULIN and TNFAIP3/A20, reverse the effects of ubiquitination by hydrolyzing linear (Met1) and Lys63 (K63) Ub moieties, respectively, from conjugated proteins...
2017: Frontiers in Immunology
https://www.readbyqxmd.com/read/28465712/a-novel-hairpin-library-based-approach-to-identify-nbs-lrr-genes-required-for-effector-triggered-hypersensitive-response-in-nicotiana-benthamiana
#15
Cyril Brendolise, Mirco Montefiori, Romain Dinis, Nemo Peeters, Roy D Storey, Erik H Rikkerink
BACKGROUND: PTI and ETI are the two major defence mechanisms in plants. ETI is triggered by the detection of pathogen effectors, or their activity, in the plant cell and most of the time involves internal receptors known as resistance (R) genes. An increasing number of R genes responsible for recognition of specific effectors have been characterised over the years; however, methods to identify R genes are often challenging and cannot always be translated to crop plants. RESULTS: We present a novel method to identify R genes responsible for the recognition of specific effectors that trigger a hypersensitive response (HR) in Nicotiana benthamiana...
2017: Plant Methods
https://www.readbyqxmd.com/read/28462531/the-interplay-of-ikk-nf-%C3%AE%C2%BAb-and-ripk1-signaling-in-the-regulation-of-cell-death-tissue-homeostasis-and-inflammation
#16
REVIEW
Vangelis Kondylis, Snehlata Kumari, Katerina Vlantis, Manolis Pasparakis
Regulated cell death pathways have important functions in host defense and tissue homeostasis. Studies in genetic mouse models provided evidence that cell death could cause inflammation in different tissues. Inhibition of RIPK3-MLKL-dependent necroptosis by FADD and caspase-8 was identified as a key mechanism preventing inflammation in epithelial barriers. Moreover, the interplay between IKK/NF-κB and RIPK1 signaling was recognized as a critical determinant of tissue homeostasis and inflammation. NEMO was shown to regulate RIPK1 kinase activity-mediated apoptosis by NF-κB-dependent and -independent functions, which are critical for averting chronic tissue injury and inflammation in the intestine and the liver...
May 2017: Immunological Reviews
https://www.readbyqxmd.com/read/28448599/simulation-of-the-dynamics-of-primary-immunodeficiencies-in-cd4-t-cells
#17
Gabriel N Teku, Mauno Vihinen
Primary immunodeficiencies (PIDs) form a large and heterogeneous group of mainly rare disorders that affect the immune system. T-cell deficiencies account for about one-tenth of PIDs, most of them being monogenic. Apart from genetic and clinical information, lots of other data are available for PID proteins and genes, including functions and interactions. Thus, it is possible to perform systems biology studies on the effects of PIDs on T-cell physiology and response. To achieve this, we reconstructed a T-cell network model based on literature mining and TPPIN, a previously published core T-cell network, and performed semi-quantitative dynamic network simulations on both normal and T-cell PID failure modes...
2017: PloS One
https://www.readbyqxmd.com/read/28445980/the-pp4r1-sub-unit-of-protein-phosphatase-pp4-is-essential-for-inhibition-of-nf-%C3%AE%C2%BAb-by-merkel-polyomavirus-small-tumour-antigen
#18
Hussein Abdul-Sada, Marietta Müller, Rajni Mehta, Rachel Toth, J Simon C Arthur, Adrian Whitehouse, Andrew Macdonald
Merkel cell carcinoma (MCC) is a highly aggressive skin cancer with a high metastatic potential. The majority of MCC cases are caused by the Merkel cell polyomavirus (MCPyV), through expression of the virus-encoded tumour antigens. Whilst mechanisms attributing tumour antigen expression to transformation are being uncovered, little is known of the mechanisms by which MCPyV persists in the host. We previously identified the MCPyV small T antigen (tAg) as a novel inhibitor of nuclear factor kappa B (NF-kB) signalling and a modulator of the host anti-viral response...
April 11, 2017: Oncotarget
https://www.readbyqxmd.com/read/28418896/nfkb-is-essential-for-activin-induced-colorectal-cancer-migration-via-upregulation-of-pi3k-mdm2-pathway
#19
Arundhati Jana, Nancy L Krett, Grace Guzman, Ahmer Khalid, Ozkan Ozden, Jonas J Staudacher, Jessica Bauer, Seung Hyun Baik, Timothy Carroll, Cemal Yazici, Barbara Jung
Colorectal cancer (CRC) remains a common and deadly cancer due to metastatic disease. Activin and TGFB (TGFβ) signaling are growth suppressive pathways that exert non-canonical pro-metastatic effects late in CRC carcinogenesis. We have recently shown that activin downregulates p21 via ubiquitination and degradation associated with enhanced cellular migration independent of SMADs. To investigate the mechanism of metastatic activin signaling, we examined activated NFkB signaling and activin ligand expression in CRC patient samples and found a strong correlation...
March 18, 2017: Oncotarget
https://www.readbyqxmd.com/read/28402272/ginkgolic-acids-inhibit-migration-in-breast-cancer-cells-by-inhibition-of-nemo-sumoylation-and-nf-%C3%AE%C2%BAb-activity
#20
Sami Hamdoun, Thomas Efferth
Ginkgolic acids (GA), a group of alkyl phenols found in crude extracts of Ginkgo biloba leaves, are known to have anticancer activity, but their mode of action is not well understood. Our aim in this study was to investigate the anti-migratory activity of seven GA against breast cancer cells and to determine the molecular mechanism behind this activity. All seven GA and their mixture inhibited wound healing in MCF-7 and MDA-MB 231 breast cancer cells. None of the compounds nor the mixture showed cytotoxicity towards the two cell lines, if tested by the resazurin assay...
March 28, 2017: Oncotarget
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