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Visiting the beamline 7.2 at SLRI Traveling grant from SLRI to attend the ASEAN Workshop on Protein Crystallography (AWPX2018)ASEAN Workshop on Protein Crystallography (AWPX2018) 30-31 August 2018 Crystallography is the fine piece of science art! It requires luck as well as patient to get a good diffraction data! the robot for the screening, they also have the available kits to do the screening 10mg/ml get per screening. LINAC - accelerate the electron (electron is generated from the electricity) The blue part is for bending the electron. underground level to boost up the energy of electrons. taking around half an hour, injecting the electron for two times a day. they will transfer the electron to the storage ring. It cost at least a million /month for sure for the electricity charge but they make very good outcomes. The scientists here are very collaborative. T 11 hours to run in the storage ring and produce the synchrotron light. they modify the ring by which

Note: Differential usage of non-homologous end-joining and homologous recombination in double strand break repair (doi: 10.1016/j.dnarep.2006.05.022 ) they mentioned that HR play dominant role in yeast, however, NHEJ contributes to DSB repair in vertebrates (my guess is that higher vertebrate genome is more complex, NHEJ is much easier to solve DSB very quick). There is the tight regulation on the switching HR and NHEJ -- events that determine the cell to go for either HR or NHEJ is cell cycle phase and DSB nature. DSB is lethal damage, if there is one unrepaired DSB, it can induce apoptosis. For the cycling cell, DSB occurs mainly during the replication. For the ionizing radiation -- i can generate break at any stages, or even the "packed chromatin" -- therefore, during the G2 and G1 which the chromosomes are packed -- it will be hard to find the homology in G2 (from sister-chromatid which is "packed") and the homology in G1 (from homology se

Note: Genetic dissection of vertebrate 53BP1: A major role in non-homologous end joining of DNA double strand breaks (doi: http://dx.doi.org/10.1016/j.dnarep.2006.03.008 ) mutation of 53BP1 in mammalian causing 1.cellular sensitivity toward radiation. 2.defect in checkpoint But DT40-53BP1(-/-) 1.intra-S phase checkpoint was normal 2.G2-M checkpoint was normal once there is the DSB -- 53BP1 is the earliest protein to recruit and form foci. In mammalian, defect in 53BP1 causes the cell cycle delays after the damage. The sequence of NHEJ; 1. Ku70/80 2.DNA-PK --> phosphorylate Artemis nuclease Artemis in IR break fixing is required more studies. Late S-G2; HR and NHEJ play role in "IR-induced" double strand break G1-early S; NHEJ is dominant AA from 203-1716 was removed. Sensitivity toward irradiation with asynchronously growing 53BP1-/- -->biphasic pattern. 53BP1(-/-) also increased the rate of HR --> this mean th

Note: Parp-1 protects homologous recombination from interference by Ku and Ligase IV in vertebrate cells (doi: 10.1038/sj.emboj.7601015) Parp-1 and Parp-2 -- responsible for SSB repair but the role of these two in HR is not clear. Using DT40 as a tool to study. DT40 has only Parp-1, no Parp-2. Parp-1(-/-) reduced the level of HR, sensitive to various DSB-inducing genotoxic agents. More sensitive when having Ku which is the DSB-binding factor. PARP1+KU70 -- proficient in initiate HR and show resistance to DSB-inducing drugs. In conclusion - having parp-1 suppress the Ku70 function and NHEJ on HR. there are so many parps (poly (ADP-ribosylation) proteins -- in mammalian, it contains 17 parps, only parp1 and parp2 act on the DNA damage response. Prarp1 and 2 interact with each other and found in the large cpx with XRCC1 and DNA-pol-beta and DNA ligase III. Evident has showed Parp1 and parp2 play role in base excision repair (BER) on damage detection, signaling and