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Relevant bibliographies by topics / NEMO-related protein

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Journal articles

Academic literature on the topic 'NEMO-related protein'

Author: Grafiati

Published: 4 June 2025

Last updated: 1 August 2025

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Journal articles on the topic "NEMO-related protein"

1

Wu, Chuan-Jin. "NEMO Family of Proteins as Polyubiquitin Receptors: Illustrating Non-Degradative Polyubiquitination’s Roles in Health and Disease." Cells 14, no. 4 (2025): 304. https://doi.org/10.3390/cells14040304.

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The IκB kinase (IKK) complex plays a central role in many signaling pathways that activate NF-κB, which turns on a battery of genes important for immune response, inflammation, and cancer development. Ubiquitination is one of the most prevalent post-translational modifications of proteins and is best known for targeting substrates for proteasomal degradation. The investigations of NF-κB signaling pathway primed the unveiling of the non-degradative roles of protein ubiquitination. The NF-κB-essential modulator (NEMO) is the IKK regulatory subunit that is essential for IKK activation by diverse

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2

Clark, Kristopher, Mark Peggie, Lorna Plater, et al. "Novel cross-talk within the IKK family controls innate immunity." Biochemical Journal 434, no. 1 (2011): 93–104. http://dx.doi.org/10.1042/bj20101701.

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Members of the IKK {IκB [inhibitor of NF-κB (nuclear factor κB)] kinase} family play a central role in innate immunity by inducing NF-κB- and IRF [IFN (interferon) regulatory factor]-dependent gene transcription programmes required for the production of pro-inflammatory cytokines and IFNs. However, the molecular mechanisms that activate these protein kinases and their complement of physiological substrates remain poorly defined. Using MRT67307, a novel inhibitor of IKKϵ/TBK1 (TANK {TRAF [TNF (tumour-necrosis-factor)-receptor-associated factor]-associated NF-κB activator}-binding kinase 1) and

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3

Tono, Chikako, Yoshihiro Takahashi, Kiminori Terui, et al. "Correction of Immunodeficiency Associated with NEMO Mutation by Umbilical Cord Stem Cell Transplantation Using a Reduced-Intensity Conditioning Regimen." Blood 108, no. 11 (2006): 5392. http://dx.doi.org/10.1182/blood.v108.11.5392.5392.

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Abstract X-linked recessive anhidrotic ectodermal dysplasia with immunodeficiency (XL-EDA-ID) is a developmental and immunologic disorder caused by hypomorphic mutations in the nuclear factor-κB essential modulator (NEMO) gene. NEMO is the regulatory subunit of the IκB kinase (IKK) complex, which phosphorylates and degrades NF-κB inhibitor α (IκBα), causing NF-κB activation. Following the identification of amorphic NEMO mutations causing familial incontinentia pigmenti (IP), hypomorphic mutations in NEMO have been identified in XL-EDA-ID patients. Affected boys are susceptible to infections wi

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4

Sarry, Morgan, Grégory Caignard, Juliette Dupré, et al. "Host-Specific Interplay between Foot-and-Mouth Disease Virus 3D Polymerase and the Type-I Interferon Pathway." Viruses 15, no. 3 (2023): 666. http://dx.doi.org/10.3390/v15030666.

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Foot-and-mouth disease (FMD) is a highly contagious viral disease affecting cloven-hoofed animals. One of the issues related to this disease is the persistence of its causative agent, foot-and-mouth disease virus (FMDV). While the mechanisms of FMDV persistence remain unclear, there are clues that it may be related to protein–protein interactions (PPI) between viral proteins and cellular proteins involved in the interferon (IFN) response. Since FMDV persistence has been described in cattle, sheep and goats but not in swine, we screened PPI involving FMDV proteins and sixteen major type-I IFN p

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5

Hansberger, Mark W., Jacquelyn A. Campbell, Pranav Danthi та ін. "IκB Kinase Subunits α and γ Are Required for Activation of NF-κB and Induction of Apoptosis by Mammalian Reovirus". Journal of Virology 81, № 3 (2006): 1360–71. http://dx.doi.org/10.1128/jvi.01860-06.

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ABSTRACT Reoviruses induce apoptosis both in cultured cells and in vivo. Apoptosis plays a major role in the pathogenesis of reovirus encephalitis and myocarditis in infected mice. Reovirus-induced apoptosis is dependent on the activation of transcription factor NF-κB and downstream cellular genes. To better understand the mechanism of NF-κB activation by reovirus, NF-κB signaling intermediates under reovirus control were investigated at the level of Rel, IκB, and IκB kinase (IKK) proteins. We found that reovirus infection leads initially to nuclear translocation of p50 and RelA, followed by d

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6

Shamilov, Rambon, Olga Vinogradova, and Brian J. Aneskievich. "The Anti-Inflammatory Protein TNIP1 Is Intrinsically Disordered with Structural Flexibility Contributed by Its AHD1-UBAN Domain." Biomolecules 10, no. 11 (2020): 1531. http://dx.doi.org/10.3390/biom10111531.

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TNFAIP3 interacting protein 1 (TNIP1) interacts with numerous non-related cellular, viral, and bacterial proteins. TNIP1 is also linked with multiple chronic inflammatory disorders on the gene and protein levels, through numerous single-nucleotide polymorphisms and reduced protein amounts. Despite the importance of TNIP1 function, there is limited investigation as to how its conformation may impact its apparent multiple roles. Hub proteins like TNIP1 are often intrinsically disordered proteins. Our initial in silico assessments suggested TNIP1 is natively unstructured, featuring numerous poten

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7

Qu, Changju, Yadong Liu, Kranthi Kunkalla, Nitin K. Agarwal та Francisco Vega. "Smoothened (SMO) Activates NF-Kb Pathway Through Activation of PKCβ/CARMA1 and TRAF6 Stabilization in Diffuse Large B-Cell Lymphoma". Blood 120, № 21 (2012): 1298. http://dx.doi.org/10.1182/blood.v120.21.1298.1298.

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Abstract Abstract 1298 Aberrant activation of hedgehog (Hh) and NF-kB pathways contribute to tumor cell growth, survival and chemotolerance in diffuse large B-cell lymphoma (DLBCL). Previously, we documented a functional crosstalk between hedgehog (Hh) and NF-kB pathways that contribute to tumor cell growth and survival in diffuse large B-cell lymphoma (DLBCL). However, the molecular mechanisms that link Hh with NF-kB pathway have not been defined. Based on that smoothened (SMO) has been associated with heterotrimeric G protein members of the Gα i family and established as a GPCRs-like protein

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8

Panezai, Jeneen, Ambereen Ghaffar, Mohammad Altamash, et al. "Periodontal Disease Augments Cardiovascular Disease Risk Biomarkers in Rheumatoid Arthritis." Biomedicines 10, no. 3 (2022): 714. http://dx.doi.org/10.3390/biomedicines10030714.

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Objectives: Periodontal disease (PD) and rheumatoid arthritis (RA) are known chronic conditions with sustained inflammation leading to osteolysis. Cardiovascular diseases (CVD) are frequent comorbidities that may arise from sustained inflammation associated with both PD and RA. In order to determine CVD risk, alterations at the molecular level need to be identified. The objective of this study, therefore, was to assess the relationship of CVD associated biomarkers in RA patients and how it is influenced by PD. Methods: The study consisted of patient (26 RA with PD, 21 RA without PD, 51 patient

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9

Sandstedt, Joakim, Karin Vargmar, Kristina Björkman, et al. "COMP (Cartilage Oligomeric Matrix Protein) Neoepitope." Arteriosclerosis, Thrombosis, and Vascular Biology 41, no. 3 (2021): 1218–28. http://dx.doi.org/10.1161/atvbaha.120.314720.

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Objective: COMP (cartilage oligomeric matrix protein) is abundantly expressed in the cardiovascular system, cartilage, and atherosclerotic plaques. We investigated if the total COMP (COMPtotal) and COMP neoepitope (COMPneo) with other cardiovascular markers and clinical parameters could identify symptomatic carotid stenosis. Approach and Results: Blood samples were collected from patients with symptomatic carotid stenosis (stenosis, n=50), patients with stroke without carotid stenosis but small plaques (plaque, n=50), and control subjects (n=50). COMPtotal and COMPneo were measured using an EL

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10

Chen, Rui, Guangda Xin, and Xiaofei Zhang. "Long non-coding RNA HCP5 serves as a ceRNA sponging miR-17-5p and miR-27a/b to regulate the pathogenesis of childhood obesity via the MAPK signaling pathway." Journal of Pediatric Endocrinology and Metabolism 32, no. 12 (2019): 1327–39. http://dx.doi.org/10.1515/jpem-2018-0432.

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Abstract Background This study aimed to investigate the completing endogenous RNA (ceRNA) network involved in childhood obesity. Methods The microarray dataset GSE9624 was downloaded from the Gene Expression Omnibus (GEO) database. Differentially expressed long non-coding RNAs (lncRNAs) (DELs) and messenger RNAs (DEMs) were isolated between the childhood obesity and non-obesity tissue samples. Then, Gene Ontology (GO) functional and the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses of isolated DEMs were performed. DELs and DEMs targeted miRNAs were predicted to construct a ce

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