Results 221 to 230 of about 666,524 (370)

NAD+‐Boosters Improve Mitochondria Quality Control In Parkinson's Disease Models Via Mitochondrial UPR

open access: yesAdvanced Science, EarlyView.
Treatment of MPTP‐incubated cells with NAD+‐boosters increase the UPRmt/mitophagy‐related mitochondria quality control (MQC). Disturbed plasma UPRmt‐mitophagy‐mediated MQC profiles in PD patient samples. NMN inhibits motor deficit and forestalls neuropathology phenotypes of PD mice, which is required the atf4‐medicated UPRmt pathway.
Shuoting Zhou   +16 more
wiley   +1 more source

Footprinting of DNA-binding proteins in intact cells [PDF]

open access: yes, 1993
Becker, Peter B.   +3 more
core   +1 more source

Glucose Deprivation‐Induced Disulfidptosis via the SLC7A11‐INF2 Axis: Pan‐Cancer Prognostic Exploration and Therapeutic Validation

open access: yesAdvanced Science, EarlyView.
Glucose deprivation or GLUT1 inhibition induces disulfidptosis in SLC7A11high ovarian cancer cells by promoting cystine accumulation, NADPH/ATP depletion, and F‐actin disulfide formation. SLC7A11 interacts with INF2 to further increase H₂O₂ levels and impair mitochondrial fission, suppressing cell migration. Targeting the SLC7A11–INF2 axis represents a
Zhenyu Song   +9 more
wiley   +1 more source

Accurate DNA Synthesis Across 8-Oxoadenine by Human PrimPol. [PDF]

open access: yesInt J Mol Sci
Boldinova EO   +4 more
europepmc   +1 more source

Topoisomerase I Inhibition in ETV4‐overexpressed Non‐Small Cell Lung Cancer Promotes Replication and Transcription Mediated R‐Loop Accumulation and DNA Damage

open access: yesAdvanced Science, EarlyView.
The oncogenic ETS factor ETV4 exerts a pleiotropic control over DNA replication both in a transcription‐dependent and ‐independent fashion in NSCLC cells. High‐ETV4 expression leads to R‐loop formation and DNA damage in response to TOP1 inhibition.
Jiaxi Zhang   +14 more
wiley   +1 more source

Unraveling the Role of MDK‐SDC4 Interaction in Pancreatic Cancer‐Associated New‐Onset Diabetes by Single‐Cell Transcriptomic Analysis

open access: yesAdvanced Science, EarlyView.
Midkine (MDK) is a mediator of the interaction between pancreatic cancer and beta cells. MDK, which originated from pancreatic ductal adenocarcinoma cells, exerted deleterious effects on paraneoplastic beta cells by binding to the SDC4 receptor on the beta cell surface and subsequently downregulating the Ras signaling pathway, thereby impairing insulin
Zengyu Feng   +7 more
wiley   +1 more source

Brief guide to gene cloning. [PDF]

open access: yesMol Cells
Hong W, Ha SG, Kwon HC, Lee SV.
europepmc   +1 more source

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