Results 221 to 230 of about 14,240,467 (389)
Editorial: Bacterial transcription factors and the cell cycle, volume II
Morigen+4 more
doaj +1 more source
Pan-Cancer Upregulation of the FOXM1 Transcription Factor. [PDF]
Pozzobon D, Bellezza A, Giorgi FM.
europepmc +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
Sox8: a multifaceted transcription factor in development and disease. [PDF]
González Alvarado MN, Aprato J.
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
The role of NRF2 transcription factor in inflammatory skin diseases. [PDF]
Salman S+3 more
europepmc +1 more source
Targeted protein degradation in oncology: novel therapeutic opportunity for solid tumours?
Current anticancer therapies are limited by the occurrence of resistance and undruggability of most proteins. Targeted protein degraders are novel, promising agents that trigger the selective degradation of previously undruggable proteins through the recruitment of the ubiquitin–proteasome machinery. Their mechanism of action raises exciting challenges,
Noé Herbel, Sophie Postel‐Vinay
wiley +1 more source
SIP2 is the master transcription factor of <i>Plasmodium</i> merozoite formation. [PDF]
Nishi T, Kaneko I, Yuda M.
europepmc +1 more source
Transcriptional modulation of transin gene expression by epidermal growth factor and transforming growth factor beta. [PDF]
Cynthia M. Machida+3 more
openalex +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