Results 11 to 20 of about 57,844 (267)

Dietary Isothiocyanates Inhibit Caco-2 Cell Proliferation and Induce G2/M Phase Cell Cycle Arrest, DNA Damage, and G2/M Checkpoint Activation [PDF]

The Journal of Nutrition, 2004
Benzyl isothiocyanate and phenethyl isothiocyanate, two aromatic phytochemicals present in substantial concentrations in edible vegetables of the genus Brassica, were investigated for their effects on Caco-2 cell proliferation. Benzyl and phenethyl isothiocyanate inhibited DNA synthesis, with 50% inhibitory concentrations of 5.1 and 2.4 micromol/L ...
Visanji, JM, Duthie, SJ, Pirie, L, Thompson, DG, Padfield, PJ.   +4 more
openaire   +3 more sources

BRCA1 Activates a G2-M Cell Cycle Checkpoint following 6-Thioguanine–Induced DNA Mismatch Damage [PDF]

Cancer Research, 2007
Abstract Human DNA mismatch repair (MMR) is involved in the response to certain chemotherapy drugs, including 6-thioguanine (6-TG). Consistently, MMR-deficient human tumor cells show resistance to 6-TG damage as manifested by a reduced G2-M arrest and decreased apoptosis.
Kazuhiko, Yamane, Jane E, Schupp, Timothy J, Kinsella   +2 more
openaire   +2 more sources

Programmed cell death 11 modulates but not entirely relies on p53-HDM2 loop to facilitate G2/M transition in colorectal cancer cells

Oncogenesis, 2023
We previously described a nucleolar protein RSL1D1 but distributed throughout the nucleus in HCT116 colorectal cancer (CRC) cells to facilitate G1/S transition by inhibiting p53 signaling.
Li Ding, Yujie Xu, Lin Xu, Chenhong Zhao, Zhiping Zhang, Jie Zhang, Kai Liao, Yuerou Chen, Jingwen Li, Xinyu Mei, Xinyue Zhang   +10 more
doaj   +1 more source

FRET-Based Sorting of Live Cells Reveals Shifted Balance between PLK1 and CDK1 Activities During Checkpoint Recovery

Cells, 2020
Cells recovering from the G2/M DNA damage checkpoint rely more on Aurora A-PLK1 signaling than cells progressing through an unperturbed G2 phase, but the reason for this discrepancy is not known.
Lorenzo Lafranchi, Erik Müllers, Dorothea Rutishauser, Arne Lindqvist   +3 more
doaj   +1 more source

Cinobufagin-Induced DNA Damage Response Activates G2/M Checkpoint and Apoptosis to Cause Selective Cytotoxicity in Cancer Cells [PDF]

Cancer Cell International, 2021
Abstract Background: Processed extracts from toad skin and parotoid gland have long been used to treat various illnesses including cancer in many Asian countries. Recent studies have uncovered a family of bufadienolides as the responsible pharmacological compounds, and the two major molecules, cinobufagin and bufalin, have been shown to possess
Jiajing Niu, Jiamei Wang, Qi Zhang, Zhihua Zou, Yushuang Ding   +4 more
openaire   +3 more sources

Identification of the first ATRIP-deficient patient and novel mutations in ATR define a clinical spectrum for ATR-ATRIP Seckel Syndrome [PDF]

, 2012
A homozygous mutational change in the Ataxia-Telangiectasia and RAD3 related (ATR) gene was previously reported in two related families displaying Seckel Syndrome (SS). Here, we provide the first identification of a Seckel Syndrome patient with mutations
A Ciccia, A Klingseisen, A Rauch, A. Malcolm R. Taylor, AD Borglum, Andrew O. M. Wilkie, D Cortez, DL Guernsey, E Griffith, E Kalay, EA Nam, Emma Hobson, EN Noensie, F Majewski, Gillian Carpenter, GK Alderton, GK Thornton, Grant S. Stewart, HL Ball, IM Ward, J Falck, J Goodship, JG Hall, Katrina Prescott, L Zou, LI Toledo, LS Bicknell, LS Bicknell, M Murga, M O'Driscoll, M Willems, Margaret Barrow, Mark O'Driscoll, Michiko Matsuse, Mohnish Suri, MS Al-Dosari, ND Lakin, Norisato Mitsutake, P Qvist, Penny A. Jeggo, Philip J. Byrd, PR Andreassen, Pradeep Vasudevan, RA Chanoux, RJ Gorlin, SA de Munnik, Sarah Walker, Siripan Limsirichaikul, Tom Stiff, Tomoo Ogi, V Paciotti, Y Namiki, Yuka Nakazawa   +52 more
core   +9 more sources

Fanconi anemia cells with unrepaired DNA damage activate components of the checkpoint recovery process [PDF]

, 2015
International audienceBACKGROUND:The FA/BRCA pathway repairs DNA interstrand crosslinks. Mutations in this pathway cause Fanconi anemia (FA), a chromosome instability syndrome with bone marrow failure and cancer predisposition.
Azpeitia, Eugenio, Cortes, Edith, Frias, Sara, Garcia-de Teresa, Benilde, Juarez, Ulises, Mendoza, Luis, Ortiz, Rocio, Ostrosky-Wegman, Patricia, Rodriguez, Alfredo, Salazar, Ana M., Sosa, David, Torres, Leda   +11 more
core   +4 more sources

Blocking CHK1 Expression Induces Apoptosis and Abrogates the G2 Checkpoint Mechanism

Neoplasia: An International Journal for Oncology Research, 2001
Checkpoint kinase 1 (Chki) is a checkpoint gene that is activated after DNA damage. It phosphorylates and inactivates the Cdc2 activating phosphatase Cdc25C. This in turn inactivates Cdc2, which leads to G2/M arrest.
Yan Luo, Shayna K. Rockow-Magnone, Paul E. Kroeger, Leigh Frost, Zehan Chen, Edward K.-H. Han, Shi-Chung Ng, Robert L. Simmer, Vincent L. Giranda   +8 more
doaj   +1 more source

Risks from low dose/dose rate radiation: what an understanding of DNA damage response mechanisms can tell us [PDF]

, 2009
The DNA damage response (DDR) mechanisms represent a vital line of defense against exogenous and endogenous DNA damage to enhance two distinct outcomes, survival and the maintenance of genomic stability. The latter is critical for cancer avoidance.
Jeggo, Peggy A.
core   +2 more sources

DNA damage-induced G2–M checkpoint activation by histone H2AX and 53BP1

Nature Cell Biology, 2002
Activation of the ataxia telangiectasia mutated (ATM) kinase triggers diverse cellular responses to ionizing radiation (IR), including the initiation of cell cycle checkpoints. Histone H2AX, p53 binding-protein 1 (53BP1) and Chk2 are targets of ATM-mediated phosphorylation, but little is known about their roles in signalling the presence of DNA damage.
Fernandez-Capetillo, Oscar, Chen, Hua-Tang, Celeste, Arkady, Ward, Irene, Romanienko, Peter J, Morales, Julio C, Naka, Kazuhito, Xia, Zhenfang, Camerini-Otero, R Daniel, Motoyama, Noboru, Carpenter, Phillip B, Bonner, William M, Chen, Junjie, Nussenzweig, André   +13 more
openaire   +3 more sources