Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học 'Respiratory Research cung cấp cho các bạn kiến thức về ngành y đề tài: " Physical and in silico approaches identify DNA-PK in a Tax DNA-damage response interactome...
Tuyển tập các báo cáo nghiên cứu về hóa học được đăng trên tạp chí sinh học quốc tế đề tài : Sodium arsenite and hyperthermia modulate cisplatin-DNA damage responses and enhance platinum accumulation in murine metastatic ovarian cancer xenograft after hyperthermic intraperitoneal chemotherapy (HIPEC)
Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học Radiation Oncology cung cấp cho các bạn kiến thức về ngành y đề tài: Enhancement of radiosensitivity in human glioblastoma cells by the DNA N-mustard alkylating agent BO-1051 through augmented and sustained DNA damage response...
Mutations in the tumor suppressor breast cancer susceptibility gene 1
(BRCA1), an important player in the DNA damage response, apoptosis,
cell cycle regulation and transcription, confer a significantly elevated life-time risk for breast and ovarian cancer.
The Nbs1 protein associates with Mre11 and Rad50 proteins to form the
Mre11–Rad50–Nbs1 complex, which plays an important role in the
intracellular signaling pathway activated in response to DNA damage.
Mutations in the genes for each of these three components of the Mre11–
Rad50–Nbs1 complex result in human diseases characterized by genomic
Genomic stability is constantly threatened by DNA damage, caused by
numerous environmental and intrinsic sources, including radiation, chemi-cals and oncogene expression. Consequently, cells have evolved a sophisti-cated signal transduction network to sense DNA damage and to mount an
appropriate DNA damage response.
The goals of chemotherapy (and radiotherapy) are to eliminate tumor cell targets by
promoting cell death. In recent years, a major focus has been placed on programmed
cell death or apoptosis as the primary mechanism of cell killing. However, tumor
cells may respond to various forms of treatment in diverse ways, only some of which
culminate in cell death and loss of clonogenic survival. In addition to apoptosis, cell
death may occur through mitotic catastrophe, autophagy (a subtype of apoptosis), or
Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học 'Respiratory Research cung cấp cho các bạn kiến thức về ngành y đề tài: "Ubiquitination of HTLV-I Tax in response to DNA damage regulates nuclear complex formation and nuclear export...
he tumor suppressor, breast cancer susceptibility gene 1 (BRCA1), plays
an integral role in the maintenance of genome stability and, in particular,
the cellular response to DNA damage. Here, the emerging role of BRCA1
in nonhomologous end-joining-mediated DNA repair following DNA dam-age will be reviewed, as well as the activation of apoptotic pathways.
Targeting BCR-ABL with Imatinib: Proof of Principle The protein product of the Philadelphia chromosome occurs in all patients with chronic myeloid leukemia (CML) and in ~30% of patients with adult acute lymphoid leukemia (ALL) and encodes the fusion protein Bcr-Abl. Although the c-Abl protooncogene is a nuclear protein whose kinase activity is tightly regulated as a part of the DNA damage response pathway (and actually induces growth arrest), the Bcr-Abl fusion protein is largely cytoplasmic with a constitutively activated tyrosine kinase domain.
The publisher assumes no responsibility for any damage or injury to persons or property arising out of the use of any materials, instructions, methods or ideas contained in the book. Publishing Process Manager Bojan Rafaj Technical Editor Teodora Smiljanic Cover Designer InTech Design Team First published April,
Hypoxic preconditioning may afford protection against subsequent lethal
hypoxia. As hypoxic tolerance induces changes in the expression of genes
involved in DNA damage and repair response pathways, we investigated
whether DNA-dependent protein kinase (DNA-PK), one of the DNA dou-ble-strand break repair proteins, could be involved in hypoxic precondi-tioning-induced protective signaling cascades.
Pyruvate is located at a crucial crossroad of cellular metabolism between
the aerobic and anaerobic pathways. Modulation of the fate of pyruvate,
in one direction or another, can be important for adaptative response to
hypoxia followed by reoxygenation.
DNA repair must take place within the context of chromatin, and it is
therefore not surprising that many aspects of both chromatin components
and proteins that modify chromatin have been implicated in this process.
One of the best-characterized chromatin modification events in DNA-dam-age responses is the phosphorylation of the SQ motif found in histone
H2A or the H2AX histone variant in higher eukaryotes. This modification
is an early response to the induction of DNA damage, and occurs in a wide
range of eukaryotic organisms, suggesting an important conserved func-tion....
Induction of p53 by the DNA damage and oncogene checkpoints.
In response to noxious stimuli, p53 and mdm2 are phosphorylated by the ataxia telangiectasia mutated (ATM) and related ATR serine/threonine kinases, as well as the immediated downstream checkpoint kinases, Chk1 and Chk2. This causes dissociation of p53 from mdm2, leading to increased p53 protein levels and transcription of genes leading to cell cycle arrest (p21Cip1/Waf1) or apoptosis (e.g., the proapoptotic Bcl-2 family members Noxa and Puma).
Cells of the budding yeast, S. cerevisiae, have for several decades now been considered
as the prototypic eukaryotic cells, ideally suited to study and uncover many
of the basic phenomena of eukaryotic life.
Silent information regulator 2 (Sir2) proteins, or sirtuins, are protein deacetylases dependent on nicotine adenine dinucleotide (NAD) and are found in organisms ranging from bacteria to humans. In eukaryotes, sirtuins regulate transcriptional repression, recombination, the celldivision cycle, microtubule organization, and cellular responses to DNA-damaging agents. Sirtuins have also been implicated in regulating the molecular mechanisms of aging. The Sir2 catalytic domain,
Tumor suppressor protein p53 plays a central role in maintaining genomic integrity
[1–3]. In unstimulated cells p53 is maintained at very low levels but in response to
DNA damage or other stress stimuli, such as hypoxia or activation of oncogenes,
p53 becomes stabilized and accumulates in the cell [4, 5]. p53 can exert its tumor
suppressor function in different ways (Fig. 1.1).
Although radiation can interfere with many cellular processes, many experts feel that a cell must undergo a double-strand DNA break from radiation in order to be killed. The factors that influence tumor cell killing include the D0 of the tumor (the dose required to deliver an average of one lethal hit to all the cells in a population), the Dq of the tumor (the threshold dose—a measure of the cell's ability to repair sublethal damage), hypoxia, tumor mass, growth fraction, and cell cycle time and phase (cells in late G1 and S are more resistant). Rate of clinical response...