Results 71 to 80 of about 823,547 (269)

A peptide puzzle

open access: yeseLife, 2018
Why does cancer develop in situations where the immune system is perfectly capable of eliminating it?
Jian Guan, Nilabh Shastri
openaire   +3 more sources

Loss of IGF‐1R impairs DNA‐PKcs recruitment to chromatin leading to defective end‐joining

open access: yesMolecular Oncology, EarlyView.
IGF‐1R promotes radioresistance by facilitating DNA‐PKcs recruitment to chromatin, enabling non‐homologous end‐joining (NHEJ) repair of double‐strand breaks. Inhibition or loss of IGF‐1R disrupts this recruitment to damage sites, driving compensatory reliance on microhomology‐mediated end‐joining (MMEJ) repair.
Matthew O. Ellis   +3 more
wiley   +1 more source

Oncogenic DMTF1β promotes cancer cell motility by regulating autophagy through ULK1 stabilization

open access: yesMolecular Oncology, EarlyView.
In the current study, we demonstrate that the oncogene DMTF1β regulates ULK1 stability by reducing its proteasomal degradation in cancer cells. This stabilization enables ULK1 to induce autophagy, which in turn facilitates cancer cell migration. Consequently, reduced DMTF1β levels lead to decreased autophagy and impaired cancer cell migration.
Jun Xu   +13 more
wiley   +1 more source

Polylactic Glycolic Acid-Mediated Delivery of Plectasin Derivative NZ2114 in Staphylococcus epidermidis Biofilms

open access: yesAntibiotics
Antimicrobial peptides (AMPs) are antibiotic candidates; however, their instability and protease susceptibility limit clinical applications. In this study, the polylactic acid–glycolic acid (PLGA)–polyvinyl alcohol (PVA) drug delivery system was screened
Xuanxuan Ma   +6 more
doaj   +1 more source

Correction to: ZIKV infection effects changes in gene splicing, isoform composition and lncRNA expression in human neural progenitor cells

open access: yesVirology Journal, 2019
In the original publication of this article [1], two grants from National Science Foundation of China and Yunnan Provincial Government (U1602226) and by National Science Foundation of China (2016YFC1200404) were omitted in the ‘Funding’ section.
Benxia Hu   +6 more
doaj   +1 more source

Epigenetic heterogeneity and plasticity in therapy‐induced tumor states through single‐cell multi‐omics

open access: yesMolecular Oncology, EarlyView.
Single‐cell multi‐omics reveals epigenetic heterogeneity across therapy‐adaptive tumor states, including quiescent/dormant, drug‐tolerant persister, and EMT‐like phenotypes. By linking regulatory features with state‐associated biomarkers, these approaches inform biomarker‐guided therapeutic strategies for evolving tumors.
Hee Jung Kim   +3 more
wiley   +1 more source

The relationship between inspiratory muscle strength and exercise tolerance in patients with coronary heart disease

open access: yesCardiology Journal
BACKGROUND: There has been insufficient research on the assessment of exercise capacity in patients with coronary heart disease (CHD) following percutaneous coronary intervention (PCI) who exhibit inspiratory muscle weakness (IMW).
Tao Shen   +4 more
doaj   +1 more source

Crystal structure of N-{N-[N-acetyl-(S)-leucyl]-(S)-leucyl}norleucinal (ALLN), an inhibitor of proteasome

open access: yesActa Crystallographica Section E: Crystallographic Communications, 2015
The title compound, C20H37N3O4, also known by the acronym ALLN, is a tripeptidic inhibitor of the proteolytic activity of the proteasomes, enzyme complexes implicated in several neurodegenerative diseases and other disorders, including cancer.
Andrzej Czerwinski   +3 more
doaj   +1 more source

PAK1 activation drives divergent resistance mechanisms to aromatase inhibition and tamoxifen in a luminal: A breast cancer model

open access: yesMolecular Oncology, EarlyView.
Breast cancer remains a major cause of cancer death in women, frequently developing endocrine therapy resistance. This study demonstrates that upregulated p21‐activated kinase 1 (PAK1) activity drives resistance to tamoxifen and long‐term estrogen deprivation in ER+ breast cancer models.
Luisa Schwarzmüller   +10 more
wiley   +1 more source

ZW4864‐mediated inhibition of the β‐catenin/BCL9/BCL9L complex reveals therapeutic potential in bladder cancer

open access: yesMolecular Oncology, EarlyView.
BCL9 and BCL9L drive bladder cancer progression by enhancing β‐catenin signaling, promoting proliferation, migration, invasion, and organoid growth. Genetic depletion of BCL9(L) suppresses malignant phenotypes, while pharmacological disruption of the β‐catenin/BCL9(L) complex with ZW4864 inhibits canonical Wnt signaling and tumor‐associated cellular ...
Roland Kotolloshi   +11 more
wiley   +1 more source

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