Results 131 to 140 of about 2,207,666 (298)

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

Engineered antibodies for the inhibition of PRRSV entry

open access: yesAnimal Diseases
Porcine reproductive and respiratory syndrome virus (PRRSV) remains a major threat to the swine industry. Owing to its high genetic variability and ability to induce immune suppression, current prevention strategies, such as vaccination, offer only ...
Siqi Zhao   +6 more
doaj   +1 more source

Viral hepatitis surveillance United States, 2018 [PDF]

open access: yes
Viral Hepatitis Surveillance \u2014 United States, 2018 is published by the Division of Viral Hepatitis, National Center for HIV/AIDS, Viral Hepatitis, STD, and TB Prevention, Centers for Disease Control and Prevention (CDC), U.S.

core   +2 more sources

Cox proportional hazards models of time until first viral failure after entry.

open access: yes, 2014
Cox proportional hazards models of time until first viral failure after entry.
Matthew Law (36008)   +6 more
core   +1 more source

Regulation of the lncRNA NEAT1 by p53‐ΔNp63 crosstalk modulates the DNA damage response and therapeutic efficacy in HNSCC

open access: yesMolecular Oncology, EarlyView.
In head and neck squamous cell carcinoma (HNSCC) p53 and p63 exert opposite roles on the transcription regulation of the lncRNA NEAT1. Under basal conditions, p53 levels are low and p63 represses NEAT1 expression. Upon genotoxic stress, p53 is rapidly induced, displacing p63 from the NEAT1 promoter leading to NEAT1 transcriptional activation and ...
Sara De Domenico   +5 more
wiley   +1 more source

Viral entry mechanisms: the role of molecular simulation in unlocking a key step in viral infections

open access: yesFEBS Open Bio
Viral infections are a major global health concern, affecting millions of people each year. Viral entry is one of the crucial stages in the infection process, but its details remain elusive. Enveloped viruses are enclosed by a lipid membrane that protects their genetic material and these viruses are linked to various human illnesses, including ...
Valério, Mariana   +4 more
openaire   +4 more sources

P4 prevents viral entry.

open access: yes
(A) PK-15 cells were infected with PRV HN1201 (MOI = 0.1) and treated with P4 (0–30 μM) for 24 h. The viral titer was determined by the TCID50 assay. (B) Mice were mock-infected, infected with PRV HN1201 (2 × 103 TCID50 per mouse), or infected with PRV ...
Guo-Yu Yang (1728175)   +4 more
core   +1 more source

Bridging the gap: a genetically validated avian chorioallantoic membrane platform for investigation of spontaneous circulating tumor cells

open access: yesMolecular Oncology, EarlyView.
We established the avian chorioallantoic membrane (CAM) assay as a scalable in vivo model for studying circulating tumor cells (CTCs). Human gastrointestinal tumors spontaneously released genetically validated CTCs that were detected across multiple platforms, demonstrating that the CAM model provides an accessible tool for investigating early cancer ...
Dennis Roth   +17 more
wiley   +1 more source

COPI is required downstream of viral entry.

open access: yes, 2013
(A) Cells were pretreated with siRNA, infected at 4°C to allow surface binding, followed by 3 hr at 25°C to resume endocytosis. Viral entry was measured by determining viral genome copies, which was almost unchanged between COPI knocked down group and ...
Qi Jin (12159)   +2 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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