Results 61 to 70 of about 599,978 (240)

NAPRT loss promotes lung tumor initiation and growth through AKT signaling independently of NAD+ biosynthesis

open access: yesMolecular Oncology, EarlyView.
Loss of NAPRT promotes lung tumor initiation and growth through a noncanonical mechanism, independent of its role in NAD+ biosynthesis. Mechanistically, NAPRT depletion activates the mTORC2‐driven AKT/β‐catenin signaling axis to enhance clonogenic and invasive phenotypes. Furthermore, lung‐specific Naprt deletion significantly increases tumor burden in
Myung Joon Oh   +11 more
wiley   +1 more source

Localized NF‐κB Inhibition Reduces Lipid Nanoparticle‐Associated Inflammation

open access: yesAdvanced Science
Lipid nanoparticles (LNPs) are widely used for nucleic acid delivery, yet their clinical utility is limited by an acute inflammatory response post‐administration. LNP‐associated inflammation (LAI) manifests as de novo inflammation in select organs (e.g.,
Carolann L. Espy   +16 more
doaj   +1 more source

LRP16 integrates into NF-κB transcriptional complex and is required for its functional activation.

open access: yesPLoS ONE, 2011
BackgroundNuclear factor κB (NF-κB)-mediated pathways have been widely implicated in cell survival, development and tumor progression. Although the molecular events of determining NF-κB translocation from cytoplasm to nucleus have been extensively ...
Zhiqiang Wu   +9 more
doaj   +1 more source

Aberrant expression of NF-κB in liver fluke associated cholangiocarcinoma: implications for targeted therapy. [PDF]

open access: yesPLoS ONE, 2014
BACKGROUND: Up-regulation and association of nuclear factor kappa B (NF-κB) with carcinogenesis and tumor progression has been reported in several malignancies. In the current study, expression of NF-κB in cholangiocarcinoma (CCA) patient tissues and its
Wunchana Seubwai   +9 more
doaj   +1 more source

Common NFKBIL2 polymorphisms and susceptibility to pneumococcal disease: a genetic association study. [PDF]

open access: yes, 2010
INTRODUCTION: Streptococcus pneumoniae remains a major global health problem and a leading cause of death in children worldwide. The factors that influence development of pneumococcal sepsis remain poorly understood, although increasing evidence points ...
Rautanen, Anna   +59 more
core   +1 more source

APOBEC3 activity and DNA polymerase‐ε deficiency are associated with distinct IDH1 R132 hotspot mutations

open access: yesMolecular Oncology, EarlyView.
Isocitrate dehydrogenase 1 (IDH1) mutations are highly recurrent in multiple human cancer types, including cholangiocarcinoma and glioma. IDH1 R132C is the most common IDH1 mutation in cholangiocarcinoma and likely arises from APOBEC3A‐ or APOBEC3B‐mediated deamination.
Kelly E. Butler   +3 more
wiley   +1 more source

NF-κB regulates neuronal ankyrin-G via a negative feedback loop

open access: yes, 2017
The axon initial segment (AIS) is a neuronal compartment defined by ankyrin-G expression. We here demonstrate that the IKK-complex co-localizes and interacts with the cytoskeletal anchor protein ankyrin-G in immunoprecipitation and proximity-ligation ...
Robert Schwamborn   +13 more
core   +3 more sources

Unique circulating miRNAome signatures captured with distinct molecular states in Lynch syndrome and sporadic colorectal cancer

open access: yesMolecular Oncology, EarlyView.
Circulating microRNA profiles distinguish nonmalignant Lynch syndrome from cancer‐associated Lynch syndrome, sporadic colorectal cancer, and healthy controls. Age‐stratified analysis reveals disease‐specific regulatory states, and a six‐miRNA panel shows concordant separation in an independent colorectal tissue cohort.
Ramadhani Salum Chambuso   +5 more
wiley   +1 more source

NF-κB response with flow and degradation.

open access: yes, 2016
(A) Representative images from confocal microscopy of NF-κB (green) and nuclear counterstain (red) following exposure to different flow times. Images were acquired at 10x magnification (scale bar = 50μm).
Scott Cooper (3373172)   +3 more
core   +1 more source

Mutant p53R273H disrupts PDPK1 homodimerization and contributes to PDPK1 activation

open access: yesMolecular Oncology, EarlyView.
How mutant p53R273H drives AKT signaling is unclear. We show that p53R273H, but not wild‐type, directly binds PDPK1 via a mutation‐dependent conformational change. This interaction disrupts inhibitory PDPK1 homodimerization and enhances AKT phosphorylation.
Mei Chee Lim   +11 more
wiley   +1 more source

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