Results 91 to 100 of about 40,147 (254)

Replicative Senescence and Cell Death [PDF]

open access: yesScience, 1995
Linskens, Maarten H.K.   +4 more
openaire   +3 more sources

Effects of IGFBP4 deficiency on human preadipocyte proliferation and differentiation through the IGF1R/AKT pathway

open access: yesFEBS Open Bio, EarlyView.
IGFBP4 knockdown (KD) impairs preadipocyte proliferation and is associated with IGF1R protein downregulation and attenuated AKT phosphorylation. The mechanisms by which IGFBP4 KD influences the IGF1R/AKT signaling pathway involve newly synthesized proteins and lysosomal degradation pathways. Created in BioRender.
Yujia Guo   +6 more
wiley   +1 more source

Pathways and pitfalls: a qualitative study of student experiences in biomedical science education

open access: yesFEBS Open Bio, EarlyView.
Biomedical science students from underrepresented backgrounds face barriers including financial strain, disrupted laboratory access and cultural exclusion. Peer networks provide vital support when institutional systems are difficult to navigate. To create inclusive learning environments and achieve academic success, educators should blend active, hands‐
Olivia J. Russell   +8 more
wiley   +1 more source

MagmaFlow: A desktop platform for artificial intelligence‐driven expression analysis

open access: yesFEBS Open Bio, EarlyView.
MagmaFlow is a free, no‐code platform for gene expression analysis. It generates interactive volcano plots, links genes to literature, pathways, and diseases, prioritizes candidates using millions of publications, identifies affected biological processes, builds network diagrams, and exports publication‐ready figures and reports for macOS and Windows ...
Carlos E. Buss   +7 more
wiley   +1 more source

Effect of terahertz irradiation on DNA damage repair in living cells

open access: yesFEBS Open Bio, EarlyView.
We investigated the effect of terahertz (THz) wave irradiation on DNA double‐strand break (DSB) repair in living cells. We found that THz irradiation enhanced DSB repair at specific frequencies, whereas heat treatment inhibited it, indicating that this effect is nonthermal and frequency‐specific.
Yuya Ueno   +3 more
wiley   +1 more source

ATZ‐1 promotes DNA replication efficiency to maintain normal meiotic function

open access: yesFEBS Open Bio, EarlyView.
Absence of ATZ‐1 interferes with meiotic DNA replication and cell cycle function via CHK‐1. This causes downstream defects associated with DNA damage and genomic integrity. Taken together, this study suggests that ATZ‐1 influences DNA replication efficiency and cell cycle function to maintain normal meiotic function.
Taylin E. Gourley   +5 more
wiley   +1 more source

Evolution‐guided yeast complementation reveals functional differences in human PSPH variants

open access: yesFEBS Open Bio, EarlyView.
Ancient genomes can help guide which human genetic variants are tested experimentally. This study applies that idea to PSPH, a gene involved in serine biosynthesis, and uses high‐throughput yeast complementation to compare variant function. The findings reveal measurable differences among selected alleles and illustrate the value of evolution‐guided ...
Mauricio Campa‐Álvarez   +6 more
wiley   +1 more source

Replicative Senescence In Vitro and In Vivo

open access: yesCroatian medical journal, 1997
Research on aging has ...
Rubelj, Ivica   +2 more
openaire   +2 more sources

Aging Is a Key Driver for Adult Acute Myeloid Leukemia

open access: yesAging and Cancer, EarlyView.
Acute myeloid leukemia (AML) is a classical age‐related hematologic malignancy, and a key driver of AML is aging, which profoundly regulates intrinsic factors such as genomic instability, epigenetic reprogramming, and metabolic dysregulation, and alters bone marrow microenvironment.
Rong Yin, Haojian Zhang
wiley   +1 more source

Mutant NPM1 in Acute Myeloid Leukemia Initiation and Maintenance

open access: yesAging and Cancer, EarlyView.
NPM1 mutations drive acute myeloid leukemia by acting as neomorphic transcriptional regulators that cooperate with Menin–MLL and XPO1 to sustain HOX/MEIS1 expression and block differentiation. Targeting these mutant‐specific transcriptional dependencies provides a rational therapeutic strategy for NPM1‐mutated AML.
Yanan Jiang   +3 more
wiley   +1 more source

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