Results 51 to 60 of about 65,805 (290)
Craniofacial Development Is Fine-Tuned by Sox2
The precise control of neural crest stem cell delamination, migration and differentiation ensures proper craniofacial and head development. Sox2 shapes the ontogeny of the cranial neural crest to ensure precision of the cell flow in the developing head. Here, we review how Sox2 orchestrates signals that control these complex developmental processes.
Nikolaos Panagiotis Mandalos+4 more
openaire +2 more sources
Evolutionary interplay between viruses and R‐loops
Viruses interact with specialized nucleic acid structures called R‐loops to influence host transcription, epigenetic states, latency, and immune evasion. This Perspective examines the roles of R‐loops in viral replication, integration, and silencing, and how viruses co‐opt or avoid these structures.
Zsolt Karányi+4 more
wiley +1 more source
Sox2 dosage: A critical determinant in the functions of Sox2 in both normal and tumor cells
AbstractThe stem cell transcription factor Sox2 is widely recognized for its many roles during normal development and cancer. Over the last several years, it has become increasingly evident that Sox2 dosage plays critical roles in both normal and malignant cells.
Ethan P. Metz, Angie Rizzino
openaire +3 more sources
Sox2 Suppresses Gastric Tumorigenesis in Mice [PDF]
Sox2 expression marks gastric stem and progenitor cells, raising important questions regarding the genes regulated by Sox2 and the role of Sox2 itself during stomach homeostasis and disease. By using ChIP-seq analysis, we have found that the majority of Sox2 targets in gastric epithelial cells are tissue specific and related to functions such as ...
Sarkar, Abby+16 more
openaire +5 more sources
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
AZD9291 has shown promise in targeted cancer therapy but is limited by resistance. In this study, we employed metabolic labeling and LC–MS/MS to profile time‐resolved nascent protein perturbations, allowing dynamic tracking of drug‐responsive proteins. We demonstrated that increased NNMT expression is associated with drug resistance, highlighting NNMT ...
Zhanwu Hou+5 more
wiley +1 more source
Self-restricted circular RNA circSOX2 suppressed the malignant progression in SOX2-amplified LUSC
Lung squamous cell carcinoma (LUSC) is a histological subtype of non-small cell lung cancer with the worse progression. SRY-Box Transcription Factor 2 (SOX2) copy number amplification (CNA) is the oncogenic driver in ~60% of patients diagnosed with LUSC.
Yingkuan Liang+8 more
doaj +1 more source
Single‐cell transcriptomics of prostate cancer patient‐derived xenografts reveals distinct features of neuroendocrine (NE) subtypes. Tumours with focal NE differentiation (NED) share transcriptional programmes with adenocarcinoma, differing from large and small cell neuroendocrine prostate cancer (NEPC). Our work defines the molecular landscape of NEPC,
Rosalia Quezada Urban+12 more
wiley +1 more source
Genetic and epigenetic modifications of Sox2 contribute to the invasive phenotype of malignant gliomas. [PDF]
We undertook this study to understand how the transcription factor Sox2 contributes to the malignant phenotype of glioblastoma multiforme (GBM), the most aggressive primary brain tumor.
Marta M Alonso+19 more
doaj +1 more source
Sox2‐dependent maintenance of mouse oligodendroglioma involves the Sox2‐mediated downregulation of Cdkn2b, Ebf1, Zfp423, and Hey2 [PDF]
AbstractCancer stem cells (CSC) are essential for tumorigenesis. The transcription factor Sox2 is overexpressed in brain gliomas, and is essential to maintain CSC. In mouse high‐grade glioma pHGG cells in culture, Sox2 deletion causes cell proliferation arrest and inability to reform tumors after transplantation in vivo; in Sox2‐deleted cells, 134 ...
Barone C.+11 more
openaire +4 more sources