Catalogue Search | MBRL
Are you sure you want to remove the book from the shelf?
{{itemTitle}}
101,627
result(s) for
"t"
Sort by:
B-cell lymphoma/leukemia 10 promotes oral cancer progression through STAT1/ATF4/S100P signaling pathway
B-cell lymphoma/leukemia 10 (BCL10) is an apoptotic regulatory protein related to advanced TNM stage and disease recurrence in oral squamous cell carcinoma (OSCC). However, the regulatory mechanism of BCL10 in OSCC progression is still unknown. Here, we showed that knockdown of endogenous BCL10 could significantly reduce cell migration and invasion abilities, retard cell proliferation by G
0
/G
1
phase accumulation and inhibit tumorigenicity
in vivo
. In molecular level, we identified S100P as a crucial downstream effector of BCL10-inhibited OSCC progression by high-throughput microarray analysis.
S100P
messenger RNA and protein expression levels were significantly diminished in silenced-BCL10 clones, and transfected S100P expression plasmids restored migration, invasion, proliferation abilities and tumorigenicity in shBCL10 transfectants. Furthermore, we provided evidence that BCL10 regulated S100P expression through signal transducers and activators of transcription 1 (STAT1) and activating transcription factor 4 (ATF4). Knockdown of BCL10 decreased S100P promoter activity, but showed no effect in truncated STAT1/ATF4 S100P promoter. In addition, we also found that the P50/P65 signaling pathway was involved in BCL10-enhanced OSCC progression. Restored S100P in silenced-BCL10 clones could markedly reverse P65 activation via outside-in signaling. Taken together, we discovered a novel axis of BCL10-regulated OSCC progression via STAT1/ATF4/S100P/P65 signaling, which could predict the prognosis of OSCC and will be beneficial for developing therapeutic strategy against advanced OSCC.
Journal Article
Every love story is a ghost story : a life of David Foster Wallace
\"The first biography of the renowned American author David Foster Wallace. Wallace was one of the most innovative and influential authors of the last twenty-five years. A writer whose distinctive style and example had a huge impact on the culture and helped give meaning to his generation in a disorienting, distressing time. In this first in-depth biography, journalist D.T. Max captures Wallace's compelling, turbulent life and times--his genius, his struggle to stay sane and happy in a difficult world, his anxiety and loneliness--as well as why he mattered as a writer and a human being\"-- Provided by publisher.
Book
Symmetry-broken Josephson junctions and superconducting diodes in magic-angle twisted bilayer graphene
The coexistence of gate-tunable superconducting, magnetic and topological orders in magic-angle twisted bilayer graphene provides opportunities for the creation of hybrid Josephson junctions. Here we report the fabrication of gate-defined symmetry-broken Josephson junctions in magic-angle twisted bilayer graphene, where the weak link is gate-tuned close to the correlated insulator state with a moiré filling factor of υ = −2. We observe a phase-shifted and asymmetric Fraunhofer pattern with a pronounced magnetic hysteresis. Our theoretical calculations of the junction weak link—with valley polarization and orbital magnetization—explain most of these unconventional features. The effects persist up to the critical temperature of 3.5 K, with magnetic hysteresis observed below 800 mK. We show how the combination of magnetization and its current-induced magnetization switching allows us to realise a programmable zero-field superconducting diode. Our results represent a major advance towards the creation of future superconducting quantum electronic devices.
Correlated electronic states in moiré matter are of great fundamental and technological interest. Here, the authors demonstrate a Josephson junction in magic-angle twisted bilayer graphene with a correlated insulator weak link, showing magnetism and programmable superconducting diode behaviour.
Journal Article
Basement membrane stiffness determines metastases formation
The basement membrane (BM) is a special type of extracellular matrix and presents the major barrier cancer cells have to overcome multiple times to form metastases. Here we show that BM stiffness is a major determinant of metastases formation in several tissues and identify netrin-4 (Net4) as a key regulator of BM stiffness. Mechanistically, our biophysical and functional analyses in combination with mathematical simulations show that Net4 softens the mechanical properties of native BMs by opening laminin node complexes, decreasing cancer cell potential to transmigrate this barrier despite creating bigger pores. Our results therefore reveal that BM stiffness is dominant over pore size, and that the mechanical properties of ‘normal’ BMs determine metastases formation and patient survival independent of cancer-mediated alterations. Thus, identifying individual Net4 protein levels within native BMs in major metastatic organs may have the potential to define patient survival even before tumour formation. The ratio of Net4 to laminin molecules determines BM stiffness, such that the more Net4, the softer the BM, thereby decreasing cancer cell invasion activity.
The basement membrane stiffness is shown to be a more dominant determinant than pore size in regulating cancer cell invasion, metastasis formation and patient survival. This stiffness is now known to be affected by the ratio of netrin-4 to laminin, with more netrin-4 leading to softer basement membranes.
Journal Article
Sofosbuvir and Velpatasvir for HCV Genotype 1, 2, 4, 5, and 6 Infection
In this phase 3 study involving patients with HCV genotype 1, 2, 4, 5, or 6 infection, including those with compensated cirrhosis, treatment with 12 weeks of sofosbuvir and velpatasvir resulted in a sustained virologic response in 99% of patients.
The hepatitis C virus (HCV), a single-stranded RNA virus of the family Flaviviridae with six major genotypes, infects up to 150 million people worldwide.
1
,
2
Chronic HCV infection causes progressive liver fibrosis, which can lead to cirrhosis, hepatic decompensation, and hepatocellular carcinoma.
3
,
4
As many as half a million people die annually from liver disease associated with chronic HCV infection.
5
In recent years, the development of drugs that directly interfere with HCV replication has revolutionized HCV treatment. There are now effective combinations of direct-acting antiviral agents for most patients, but in choosing an appropriate regimen, clinicians must take into account . . .
Journal Article