Random Records

As far as I have read through the literature on cancer and cellular signaling; normal --> dysplasia (lesion) -->cancer It is not surprising that why tumor has heterogeneity and it is hard to beat. DNA is very prone to be mutated all the times, either external or internal sources. The internal source, for example, is from the metabolites being produced in the cell to keep the cell alive - the most important term that we have heard of is reactive oxygen species (ROS). Most of the macromolecules are rich in electron, one of which is DNA. Therefore, the DNA can be oxidized and their sequences are inevitably changed. I would say homeostasis is the term which anabolic system is equal to catabolic system. However, since our body has linked with the external environment, there ain't ways that the homeostasis will not be disturbed (for example, there might be the day that PM2.5 reaches to the hazardous level . Once the system has been interrupted, the cell will manage itself to

Note: Gamma-H2AX in recognition and signaling of DNA double-strand breaks in the context of chromatin (doi: 10.1093/nar/gkn550) Three PI3KK can phosphorylate H2Ax; ATM, ATR and DNA-PK – each requires partner to recognize the break differently. MRN-ATM (heterochromatin region, S/G2-phase), ATRIP-ATR (stalled replication fork or bulk-damage entering to S-phase) and KU70/80-DNA-PK (occur throughout cell cycle). Scoring gH2Ax requires attention since it is not solely represented DSB. Remaining of gH2Ax foci does not mean the DSB has not been fixed. It may remain there to signal the HR to do more additional repair after seal with NHEJ, or the phosphatase system might be malfunction. The further condensation of the 30nm fiber as well as higher levels of chromatin condensation, which culminate with the 10 000-fold compaction of the stretched DNA fiber in the 700nm metaphase chromosomes, are less well understood, but are facilitated by the linker histone H1 and condensins. By

Note: DNA Damage Foci: Meaning and Significance (doi: 10.1002/em.21944) Basically, it can reflect DNA damage response but it cannot be solely related to DSB. (ionizing) radiation-induced foci (IRIF or RIF) or DNA repair foci. the histone variant H2AX which gets phosphorylated at its C-terminal Ser-139 residue by the DNA damage-activated kinases ATM, ATR, and DNA-PK, to form gH2AX. gH2AX then acts as a docking station for other DNA damage signaling factors such as MDC1 and 53BP1 which accumulate to form foci in a histone-modification-dependent manner. Foci can also be analysed using fluorescent protein fusion constructs, enabling foci formation and loss  to be monitored in live cells. As scoring is severely influenced by staining quality and imaging characteristics, it is good practice to include positive and negative reference samples which help confirm the validity and reproducibility of the results obtained in a particular experiment. Intensity-based approaches such as

I have attended two meetings and they are all very fruitful for me. The most stunning one is the one which I would say 'yin and yang' - sustainable vs. capitalized type. For the sustainable is very challenging and it is against the mainstream of capitalization. It relies on the belief and attitude to push the sustainable one to the end. Enoughness level is really diverse and also lifestyle is different in each people. The world is dynamics - how do we live happily and peacefully with the disruptive era? # Savechumphoncabana PS. Those two meetings remind me of the story of the Bangkokian museum.

Note for: ATM kinase: Much more than a DNA damage responsive protein   (doi: 10.1016/j.dnarep.2015.12.009) It is a very large protein and post-translational modifications are the mechanism which ATM is regulated. Besides, one protein can either regulate ATM and be a downstream substrate of ATM! ATM has so many cellular roles not only DNA damage sensor. It can sense the redox status within the cell and the environment affects the structure of ATM which later control its activity! Sound to me, both ATM substrates and the proteins that control the ATM might be different in each cell type.  ATM -- multifunctional protein kinase during past two decades, established and predominant role in DNA damage response, to help in maintaining overall functional integrity of cells; oxidative stress, metabolic syndrome, mitochondrial dysfunction as well as neurodegeneration. several proteins which might be acting as substrates of ATM. effective regulatory controls within the ATM-medi