Results 211 to 220 of about 3,456,235 (361)
This study used longitudinal transcriptomics and gene‐pattern classification to uncover patient‐specific mechanisms of chemotherapy resistance in breast cancer. Findings reveal preexisting drug‐tolerant states in primary tumors and diverse gene rewiring patterns across patients, converging on a few dysregulated functional modules. Despite receiving the
Maya Dadiani+14 more
wiley +1 more source
Integrated miRNA-mRNA Profiling of C2C12 Myoblasts Indicates Regulatory Interactions Involved in Proliferation and Differentiation. [PDF]
Chang X, Ma J.
europepmc +1 more source
Correlation between fission-time and culture-age in the Proliferation of Bacteria
Jun Hirano
openalex +2 more sources
CELL PROLIFERATION AND SPECIALIZATION DURING ENDOCHONDRAL OSTEOGENESIS IN YOUNG RATS [PDF]
Richard W. Young
openalex +1 more source
B‐cell chronic lymphocytic leukemia (B‐CLL) and monoclonal B‐cell lymphocytosis (MBL) show altered proteomes and phosphoproteomes, analyzed using mass spectrometry, protein microarrays, and western blotting. Identifying 2970 proteins and 316 phosphoproteins, including 55 novel phosphopeptides, we reveal BCR and NF‐kβ/STAT3 signaling in disease ...
Paula Díez+17 more
wiley +1 more source
H3K18 lactylation-mediated Ythdf2 activation restrains mouse female germline stem cell proliferation via promoting Ets1 mRNA degradation. [PDF]
Wu Y+9 more
europepmc +1 more source
Ubiquitination of transcription factors in cancer: unveiling therapeutic potential
In cancer, dysregulated ubiquitination of transcription factors contributes to the uncontrolled growth and survival characteristics of tumors. Tumor suppressors are degraded by aberrant ubiquitination, or oncogenic transcription factors gain stability through ubiquitination, thereby promoting tumorigenesis.
Dongha Kim, Hye Jin Nam, Sung Hee Baek
wiley +1 more source
MiR- 223 alleviates the heat-stress-induced inhibition of cell proliferation by targeting PRDM1. [PDF]
Xia S+10 more
europepmc +1 more source
Nuclear prothymosin α inhibits epithelial‐mesenchymal transition (EMT) in lung cancer by increasing Smad7 acetylation and competing with Smad2 for binding to SNAI1, TWIST1, and ZEB1 promoters. In early‐stage cancer, ProT suppresses TGF‐β‐induced EMT, while its loss in the nucleus in late‐stage cancer leads to enhanced EMT and poor prognosis.
Liyun Chen+12 more
wiley +1 more source