Results 81 to 90 of about 6,549,693 (278)

The VHL tumor suppressor at the crossroad of protein folding, aggregation, and cancer

open access: yesMolecular Oncology, EarlyView.
Mutations, environmental stress, and chaperone dysfunction can destabilize pVHL, promoting its conversion from the native folded state into amyloid‐like assemblies. This transition may contribute to protein storage, cell dormancy, survival, and drug resistance.
Lara Abad   +2 more
wiley   +1 more source

The Cell Cycle, Mitosis and Meiosis

open access: yes, 2010
This OER consists of an instructional sheet produced by GENIE CETL in the Department of Genetics. This learning material is about the life cycle of a cell and the series of stages by which genetic materials are duplicated and partitioned to produce two ...
GENIE CETL
core  

Targeting the cell cycle in breast cancer: towards the next phase

open access: yes, 2018
© 2018 Informa UK Limited, trading as Taylor & Francis Group. Deregulation of the cell cycle is a hallmark of cancer that enables limitless cell division.
I Soria-Bretones   +7 more
core   +1 more source

Regulation of the lncRNA NEAT1 by p53‐ΔNp63 crosstalk modulates the DNA damage response and therapeutic efficacy in HNSCC

open access: yesMolecular Oncology, EarlyView.
In head and neck squamous cell carcinoma (HNSCC) p53 and p63 exert opposite roles on the transcription regulation of the lncRNA NEAT1. Under basal conditions, p53 levels are low and p63 represses NEAT1 expression. Upon genotoxic stress, p53 is rapidly induced, displacing p63 from the NEAT1 promoter leading to NEAT1 transcriptional activation and ...
Sara De Domenico   +5 more
wiley   +1 more source

Cell cycle checkpoint revolution: targeted therapies in the fight against malignant tumors

open access: yesFrontiers in Pharmacology
Malignant tumors are among the most important causes of death worldwide. The pathogenesis of a malignant tumor is complex and has not been fully elucidated. Studies have shown that such pathogenesis is related to abnormal cell cycle progression.
Guangming Song   +10 more
doaj   +1 more source

EZH2 enables germinal centre formation through epigenetic silencing of CDKN1A and an Rb-E2F1 feedback loop

open access: yesNature Communications, 2017
The histone methyltransferase EZH2 silences genes by generating H3K27me3 marks. Here the authors use a 3D GC organoid and show EZH2 mediates germinal centre (GC) formation through epigenetic silencing of CDKN1A and release of cell cycle checkpoints.
Wendy Béguelin   +10 more
doaj   +1 more source

Fate specification and tissue-specific cell cycle control of the Caenorhabditis elegans intestine [PDF]

open access: yes, 2010
Coordination between cell fate specification and cell cycle control in multicellular organisms is essential to regulate cell numbers in tissues and organs during development, and its failure may lead to oncogenesis.
Segref, Alexandra   +9 more
core   +1 more source

SPHINX31 acts as a SRPK1 inhibitor targeting the ATR/DNA‐PKcs/CHK1 replicative checkpoint to inhibit cell growth in non‐small cell lung cancer

open access: yesMolecular Oncology, EarlyView.
The kinase SRPK1 directly interacts with the protein TOPBP1 and regulates the pre‐mRNA splicing of WIZ thereby contributing to the activation of the ATR/CHK1 replicative checkpoint in response to replicative stress. This allows cancer cells' genomic stability and survival.
Amani Shreim   +17 more
wiley   +1 more source

Aquaporin‐3 and aquaporin‐5 impact the development of pancreatic ductal adenocarcinoma spheroids

open access: yesFEBS Open Bio, EarlyView.
Schematic representation of the role of aquaporin‐3 (AQP3) and aquaporin‐5 (AQP5) in pancreatic ductal adenocarcinoma (PDAC). Both proteins are upregulated in PDAC and are associated with tumor progression and metastatic potential. Silencing AQP3 or AQP5 in PDAC spheroids results in decreased diameter, area, and overall growth, underscoring their key ...
Catarina Pimpão   +3 more
wiley   +1 more source

Cell cycle control and its modulation in HPV infected cells [PDF]

open access: yes, 2010
A key effect of human papillomavirus (HPV) infection is to disrupt the normal cell cycle in order to subvert the cellular DNA replication machinery. Morphologically, condylomata induced by high and low risk HPV types cannot be distinguished and many ...
Lyman, Rachel C.
core   +2 more sources

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