Results 71 to 80 of about 1,665,599 (197)

The Chromosome Passenger Complex (CPC) Components and Its Associated Pathways Are Promising Candidates to Differentiate Between Normosensitive and Radiosensitive ATM-Mutated Cells

Biomarker Insights
Background: Sensitivity to ionizing radiation differs between individuals, but there is a limited understanding of the biological mechanisms that account for these variations.
Anne Dietz, Prabal Subedi, Omid Azimzadeh, Lukas Duchrow, Felix Kaestle, Juliane Paetzold, Sarah Katharina Payer, Sabine Hornhardt, Christine von Toerne, Stefanie M Hauck, Bettina Kempkes, Cornelia Kuklik-Roos, Danielle Brandes, Arndt Borkhardt, Simone Moertl, Maria Gomolka   +15 more
doaj   +1 more source

The Ataxia Telangiectasia Mutated and Cyclin D3 Proteins Cooperate To Help Enforce TCRβ and IgH Allelic Exclusion [PDF]

The Journal of Immunology, 2014
Abstract Coordination of V rearrangements between loci on homologous chromosomes is critical for Ig and TCR allelic exclusion. The Ataxia Telangietasia mutated (ATM) protein kinase promotes DNA repair and activates checkpoints to suppress aberrant Ig and TCR rearrangements.
Natalie C, Steinel, Megan R, Fisher, Katherine S, Yang-Iott, Craig H, Bassing   +3 more
openaire   +2 more sources

Chronobiology of Cancer: How Aging Fuels Oncogenesis at the Molecular Level

Aging and Cancer, EarlyView.
This graphical abstract illustrates the key biological pathways linking aging with cancer development and progression. In the upper left, cumulative exposure to ultraviolet radiation, toxins, and reactive oxygen species (ROS) causes DNA damage and genomic instability, whereas age‐related decline in repair mechanisms, such as ATM/ATR, BER, and NER ...
Anu Singh, Aroonima Misra, Sufian Zaheer
wiley   +1 more source

Oxidative stress is responsible for deficient survival and dendritogenesis in Purkinje neurons from ataxia-telangiectasia mutated mutant mice [PDF]

, 2003
Atm gene-disrupted mice recapitulate the majority of characteristics observed in patients with the genetic disorder ataxia-telangiectasia (A-T). However, although they exhibit defects in neuromotor function and a distinct neurological phenotype, they do ...
Cheng Peng, Martin F. Lavin, Philip Chen, Steven Bottle, Watters, Dianne, Lavin, Martin F., Lavin, Martin, Spring, Kevin, Dianne Watters, Luff, John, Furuya, Shigeki, John Luff, Kevin Spring, Chen, Philip, Peng, Cheng, Bottle, Steven, Shigeki Furuya   +16 more
core   +1 more source

Compound Heterozygous ATM Variants Cause Adolescent-Onset Cerebellar and Extrapyramidal Disease Without Telangiectasia in a Consanguineous Pakistani Family

Genetics Research
Ataxia–telangiectasia (A–T) is a heterogeneous genetic disorder with a recessive mode of inheritance resulting from biallelic variants in the A–T mutated gene (ATM).
Faiza Aslam, Weizhen Ji, Lauren Jeffries, Anant Wadhwa, Monica Konstantino, Muhammad Noman, Nigel S. Bamford, Emily Mis, Saquib A. Lakhani, Sadaf Naz   +9 more
doaj   +1 more source

A Macrohistone Variant Links Dynamic Chromatin Compaction to BRCA1-Dependent Genome Maintenance

Cell Reports, 2014
Appropriate DNA double-strand break (DSB) repair factor choice is essential for ensuring accurate repair outcome and genomic integrity. The factors that regulate this process remain poorly understood. Here, we identify two repressive chromatin components,
Simran Khurana, Michael J. Kruhlak, Jeongkyu Kim, Andy D. Tran, Jinping Liu, Katherine Nyswaner, Lei Shi, Parthav Jailwala, Myong-Hee Sung, Ofir Hakim, Philipp Oberdoerffer   +10 more
doaj   +1 more source

Novel function of HATs and HDACs in homologous recombination through acetylation of human RAD52 at double-strand break sites. [PDF]

PLoS Genetics, 2018
The p300 and CBP histone acetyltransferases are recruited to DNA double-strand break (DSB) sites where they induce histone acetylation, thereby influencing the chromatin structure and DNA repair process.
Takeshi Yasuda, Wataru Kagawa, Tomoo Ogi, Takamitsu A Kato, Takehiro Suzuki, Naoshi Dohmae, Kazuya Takizawa, Yuka Nakazawa, Matthew D Genet, Mika Saotome, Michio Hama, Teruaki Konishi, Nakako Izumi Nakajima, Masaharu Hazawa, Masanori Tomita, Manabu Koike, Katsuko Noshiro, Kenichi Tomiyama, Chizuka Obara, Takaya Gotoh, Ayako Ui, Akira Fujimori, Fumiaki Nakayama, Fumio Hanaoka, Kaoru Sugasawa, Ryuichi Okayasu, Penny A Jeggo, Katsushi Tajima   +27 more
doaj   +1 more source

A splicing mutation affecting expression of ataxia–telangiectasia and Rad3–related protein (ATR) results in Seckel syndrome [PDF]

Nature Genetics, 2003
Seckel syndrome (OMIM 210600) is an autosomal recessive disorder characterized by intrauterine growth retardation, dwarfism, microcephaly and mental retardation. Clinically, Seckel syndrome shares features in common with disorders involving impaired DNA-damage responses, such as Nijmegen breakage syndrome (OMIM 251260) and LIG4 syndrome (OMIM 606593 ...
O'Driscoll M, Ruiz-Perez VL, Woods CG, Jeggo PA, Goodship JA   +4 more
openaire   +3 more sources

Glycosylated dendrimer nanoamplifiers hijack DNA damage‐immune crosstalk for enhanced dual‐track therapy of orthotopic glioblastoma

BMEMat, EarlyView.
A glycosylated dendrimer nanoamplifier hijacks DNA damage‐immune crosstalk for enhanced radio‐immunotherapy of glioblastoma. The responsive release of demethylcantharidin simultaneously blocks repair‐mediated resistance by inhibiting DNA repair and overcomes adaptive immune resistance.
Cong Song, Binghan Liu, Junjie Liu, Ce Li, Wenqing Man, Xurui Sun, Chang Yuan, Yanjun Wang, Hong Pan, Shuanglian Wang, Zhiming Zheng   +10 more
wiley   +1 more source

MOLECULAR AND CELLULAR CHANGES IN ARTERIAL FUNCTION OVER THE LIFE COURSE – FROM ACCELERATED AGEING TO CALCIFICATION

Artery Research, 2018
Vascular stiffening and calcification are hallmarks of ageing and these pathologies are accelerated in patients with diabetes and renal failure. Emerging evidence has defined a role for nuclear lamina defects and the DNA damage response in driving ...
Catherine M. Shanahan
doaj   +1 more source