Results 31 to 40 of about 12,825 (214)

Loss of IGF‐1R impairs DNA‐PKcs recruitment to chromatin leading to defective end‐joining

open access: yesMolecular Oncology, EarlyView.
IGF‐1R promotes radioresistance by facilitating DNA‐PKcs recruitment to chromatin, enabling non‐homologous end‐joining (NHEJ) repair of double‐strand breaks. Inhibition or loss of IGF‐1R disrupts this recruitment to damage sites, driving compensatory reliance on microhomology‐mediated end‐joining (MMEJ) repair.
Matthew O. Ellis   +3 more
wiley   +1 more source

Polimorfismo -308G>A del gen codificante del factor de necrosis tumoral alfa, periodontitis y síndrome coronario agudo

open access: yesCorreo Científico Médico, 2023
Introducción: La periodontitis y las enfermedades cardiovasculares de origen isquémico se han convertido en un serio problema para la salud pública a nivel mundial. Estas enfermedades tienen etiología multifactorial con un importante componente genético.
Maricelys Leonor Martínez Pérez   +2 more
doaj  

Guidelines on the diagnosis and management of the progressive ataxias [PDF]

open access: yes, 2019
The progressive ataxias are a group of rare and complicated neurological disorders, knowledge of which is often poor among healthcare professionals (HCPs).
Bonney, H   +14 more
core   +1 more source

Cancer‐associated mutations in endometriosis reframe a benign disease through molecular oncology

open access: yesMolecular Oncology, EarlyView.
This review aims to comprehensively analyse cancer‐associated somatic mutations (CAMs) present in endometriotic lesions, emphasizing their biological roles, spatial distribution and implications for translational applications in medicine. By contextualizing a benign state within a genomic framework, this analysis seeks to establish its value as a ...
Clarissa Mujacic   +15 more
wiley   +1 more source

Ataxias adquiridas: clasificación y enfoque diagnóstico

open access: yes, 2022
[[EN] Acquired ataxias are a group of heterogeneous diseases that includes those with autoimmune (paraneoplastic and non-paraneoplastic), toxic, infectious, vitamin deficiency, tumor and vascular origin.
Adarmes-Gómez, Astrid
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

Movement Disorders in Spinocerebellar Ataxias

open access: yes, 2011
Universidade Federal de São Paulo, Dept Neurol & Neurosurg, Div Gen Neurol & Ataxias, São Paulo, BrazilUniversidade Federal de São Paulo, Dept Neurol & Neurosurg, Div Gen Neurol & Ataxias, São Paulo, BrazilWeb of ...
Pedroso, Jose Luiz [UNIFESP]   +7 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

Precision Medicine in Ataxias

open access: yes, 2022
Trabajo presentado en Ataxias, one world, celebrado en modalidad virtual el 25 de septiembre de ...
Sánchez-Alcázar, José Antonio
core  

Treatment with KCL‐286, a first‐in‐class retinoic acid receptor‐β (RARβ) agonist, ameliorates neuronal DNA damage and inflammation in a mouse model of Alzheimer's disease

open access: yesFEBS Open Bio, EarlyView.
Repair of neuronal DNA damage in Alzheimer's disease by KCL‐286. (A) Amyloid‐β oligomers and plaques impair neuronal DNA repair pathways, leading to DNA double‐strand breaks and glial activation. (B) KCL‐286 activates RARβ/RXR signalling via retinoic acid response elements (RAREs), associated with increased BRCA1 expression, enhanced DNA repair and ...
Natasha Hill   +6 more
wiley   +1 more source

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