Results 131 to 140 of about 198,463 (306)

p53 directly regulates the glycosidase FUCA1 to promote chemotherapy-induced cell death [PDF]

open access: yes, 2016
p53 is a central factor in tumor suppression as exemplified by its frequent loss in human cancer. p53 exerts its tumor suppressive effects in multiple ways, but the ability to invoke the eradication of damaged cells by programmed cell death is considered
Baudot, Alice D.   +5 more
core   +2 more sources

Evaluation of the Dual Impact of Nanotechnologies on Health and Environment Through Alternative Bridging Models

open access: yesAdvanced Healthcare Materials, EarlyView.
This review explores how alternative invertebrate and small‐vertebrate models advance the evaluation of nanomaterials across medicine and environmental science. By bridging cellular and organismal levels, these models enable integrated assessment of toxicity, biodistribution, and therapeutic performance.
Marie Celine Lefevre   +3 more
wiley   +1 more source

Wild type p53 function in p53Y220C mutant harboring cells by treatment with Ashwagandha derived anticancer withanolides: bioinformatics and experimental evidence

open access: yesJournal of Experimental & Clinical Cancer Research, 2019
Background Tumor suppressor p53 protein is frequently mutated in a large majority of cancers. These mutations induce local or global changes in protein structure thereby affecting its binding to DNA.
Durai Sundar   +9 more
doaj   +1 more source

Citron Kinase Deficiency Leads to Chromosomal Instability and TP53-Sensitive Microcephaly [PDF]

open access: yes, 2017
Mutations in citron (CIT), leading to loss or inactivation of the citron kinase protein (CITK), cause primary microcephaly in humans and rodents, associated with cytokinesis failure and apoptosis in neural progenitors.
Alessandra Maria Adelaide, Chiotto   +21 more
core   +3 more sources

Strawberry Notch 1 Acts as a Transcriptional Regulator Driving Oncogenic Programs in Liver Carcinogenesis

open access: yesAdvanced Science, EarlyView.
This study reports that SBNO1 protein is upregulated in several cancer entities. SBNO1 protein interacts with the basal transcription factor TFIID via TAF4, enabling its recruitment to transcription start sites and the modulation of target gene expression.
Sarah Fritzsche   +21 more
wiley   +1 more source

p53 Reactivation by the small molecule RITA: molecular mechanisms [PDF]

open access: yes, 2011
Inactivation of the tumor suppressor p53 is essential for the development and maintenance of cancer cells. Therefore, reactivation of p53 appears to be a promising strategy for anti-cancer therapy. We have previously identified the small molecule RITA
Grinkevich, Vera
core   +1 more source

Stochastic Nanoscale Biophysical Cues as a Basis for the Induction of Glioblastoma‐Like Transcriptional Programs in Astrocytes

open access: yesAdvanced Science, EarlyView.
Stochastic nanoscale physical cues induce glioblastoma (GBM)‐associated transcriptional traits in naïve astrocytes leading to spontaneous formation of spheroids. Cells within spheroids express activated‐MMP2 and a differential gene expression pattern involving P53 and NOTCH3, providing evidence for a role for changes in brain topography, as observed in
Laurent Starck   +8 more
wiley   +1 more source

Mutated TP53 is a marker of increased VEGF expression: analysis of 7,525 pan-cancer tissues. [PDF]

open access: yes, 2020
Anti-angiogenic therapies are an important class of anti-cancer treatment drugs. However, their efficacy is limited to certain tumors and would benefit from identifying a biomarker predictive of therapeutic response.
Boichard, Amélie   +2 more
core  

Roles of tumor suppressors in regulating tumor-associated inflammation. [PDF]

open access: yes, 2014
Loss or silencing of tumor suppressors (TSs) promotes neoplastic transformation and malignant progression. To date, most work on TS has focused on their cell autonomous effects.
Karin, M, Yang, L
core   +1 more source

CDK4/6 Inhibition Induces CD8+ T Cell Antitumor Immunity via MIF‐Induced Functional Orchestration of Tumor‐Associated Macrophages

open access: yesAdvanced Science, EarlyView.
CDK4/6 inhibition promotes CD8+ T cell expansion through tumor‐macrophage crosstalk by activating HIF‐1α and enhancing MIF‐CD44/CD74 signaling. This reprograms TAMs to boost MHC‐I antigen presentation, and CDK4/6 inhibitor‐trained M1 TAM supernatant therapy synergizes with low‐dose PD‐1 blockade to restore antitumor immunity.
Lin He   +17 more
wiley   +1 more source

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