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Just google it and save for the record; Biotech (drug discovery); http://www.biotec.or.th/en/index.php/global-networks/biotec-novartis-drug-discovery-partnership Mahidol University (drug discovery); http://ecdd.sc.mahidol.ac.th/ http://sisyspharm.org/index.php/en/ Thammasat University (drug discovery); http://www.sat.tu.ac.th/tuddd/tuddd_main.php Chulalongkorn University (drug discovery); https://www.research.chula.ac.th/chula4dr-eng/ Prince Songkla University (drug delivery); http://dds.pharmacy.psu.ac.th/index.php Pharmaceutical Research and Manufacturers Association http://www.prema.or.th/www/index.php?lan=th Few slides that I got from google searching Source:  https://apac-asia.com/images/achievements/pdf/6th/03-03.pdf Where else that I miss?

Two papers that I have read; one is the short communication which briefs the major finding of RNF138 contributing to DNA repair. The other paper is the original paper which performed the experiments to show that RNF138 is the new finding regulator of HR. Note for – 1.   RNF138 joins the HR team (doi: 10.1038/ncb3262) 2.   The RNF138 E3 ligase displaces Ku to promote DNA end resection and regulate DNA repair  pathway choice (doi: 10.1038/ncb3259)   RNF138 will be a good target for the choice switching between HR and NHEJ. Protein modification by ubiquitin has a central role in regulating DSB repair. Each cell cycle fate, will be controlled by different sets of protein through the ubiquitination process, like in this case, it is showed that RNF138 promote Ku ubiquitination during S and G2 phase when resection is operational. Cell cycle stage and DNA end resection are believed to regulate the commitment to HR repair. This study identifies RNF138 (Ub-E3 ligase) which reg

เมื่อดีเอ็นเอภายในเซลล์ถูกทำลาย เซลล์ในร่างกายเราจะมีการรับรู้โดยทันทีว่ามีความเสียหายเกิดขึ้น และจะส่งสัญญาณต่อไปยังพรรคพวก เพื่อให้มาซ่อมแซมความเสียหายดังกล่าว ซึ่งโดยปกติแล้วมันจะมีอยู่สามกระบวนการหลังจากที่เซลล์มีการรับรู้ว่ามีความเสียหาบระดับดีเอ็นเอเกิดขึ้น นั่นคือ 1. ในกรณีที่เซลล์มีการแบ่งตัว เซลล์จะส่งสัญญาบอกว่า เจ้า! จงหยุดแบ่งตัวก่อน ขอเวลาข้าซ่อมแซมรหัสพันธุกรรมอันล้ำค่าก่อน มิฉะนั้นแล้วข้อมูลที่ถูกส่งผ่านไปยังรุ่นลูก อาจมีความผิดพลาดได้ 2. เมื่อเซลล์หยุดการแบ่งตัว ไม่มีกิจกรรมอื่นใด เซลล์ก็มีพลังงานพอที่จะซ่อมแซมความเสียหายที่เกิดขึ้น ทั้งจากตัวเร้าที่มาจากภายนอก หรือภายใน 3. แต่ถ้าเมื่อใดก็ตาม ความเสียหายดังกล่าว มันยากเกินที่จะเยียวยาเหลือเกิน จะอยู่ต่อไปก็ไม่เกิดประโยชน์อะไร เมื่อพิจารณาแล้วว่าความเสียหายนั้น ยากที่จะเกิดการแก้ไข การยอมพลีชีพ ย่อมจะมีประโยชน์มากกว่าการทนอยู่แบบมีความผิดปกติอยู่ข้างใน ซึ่งเสี่ยงต่อการสูญเสียการควบคุมการเจริญเติบโต ซึ่งต่อมาก็กลายเป็นก้อนเนื่องอก หรือมะเร็งโดยที่สุด! จบ.

Current research: Our current research group is focusing on the DNA repair pathways, especially, DNA double-strand break repairs. DNA repair is a vital mechanism and its malfunction can cause cancer. In contrast, the cancer cells also exploit the repair mechanism to facilitate tumor growth. Since the DNA repair mechanism is complex, thus, there are numbers of genes/proteins which their precise role in carcinogenesis is elusive. To explore the function of novel DNA double-strand break repair genes/proteins in carcinogenesis, our research group have used the reverse genetic approach to understand the mechanism. Because the targeted-therapy in the DNA repair pathway is very expensive and limited, we would like to search for the new lead compounds which could be developed in our country. We are now setting up the biosensor based on DNA double-strand break repair and using the high throughput screening technology (HST) to find the candidate compounds that are from local endophytic extract

Note for: Endophytic fungi with anti-microbial, anti-cancer and anti-malarial activities isolated from Thai medicinal plants (doi: 10.1023/B:WIBI.0000023832.27679.a8) 1.81 Thai medicinal plants! 2.4 geographical regions of Thailand 3.isolate endophytes and investigating biological activity 4.582 pure isolates, 360 distinct fungi morphologic culture 1. malt Czapek broth 2. yeast extract sucrose broth 5.Biological activities include; Antimicrobial/viral - M. tuberculosis, P. falciparum, Herpes simplex virus type1 Anticancer activity - human oral epidermoid carcinoma, breast cancer cells 6.Type of media affects the bioactivity profile 7.obstacle of this study -- fungi could not produce spore --> could not identify. Sample collection; Ubonratchathani, Nakornratchasima, Chiangmai, Songkla Crude extract after dry --> 80 mg/ml - 1 g/ml in DMSO depending on solubility. Tuberculosis test Final concentration --> 800 ug/ml (making the serial 2

Note for: The Notch inhibitor cowanin accelerates nicastrin degradation (doi: 10.1038/s41598-018-23698-4) Notch alteration contributes to carcinogenesis. Therefore, it could be used as the target to treat the cancer. Using cell-based system to screen compound from Garcinia speciosa. 1/12 was found to inhibit notch signaling pw. HES1 and HES5 are the targets. Cowanin decreases HES1 and HES5 protein level. Cytotoxic to leukemic HPB-ALL. Notch signaling - many fundamental process; 1.proliferation 2.stem cell maintenance 3.differentiation (well just like wnt signaling pw) It is important for neuronal diff. It has been regulated through hairy and enhancer of split 1 ( HES1 ), HES5 and HES related ( HESR/HEY ) family genes. Aberration in Notch signaling participates in both multiple hematologic and solid malignancies. Notch signaling is activated by interaction between the ligand-expressing cell and the signal-receiving cell. Various Notch inhibitors;

Note: Cancer TARGETases: DSB repair as a pharmacological target (doi: 10.1016/j.pharmthera.2016.02.007) DNA is not just the plain sequences which contain ATCG but we have to consider how it form the secondary structure within the strand, how it folds with the histone --> these are related to replication as well as DNA repair process. Some studies show that heterochromatin (tight) and euchromatin (loose) has been repaired by different repair mechanisms. DNA repair, esp. DSB is good targets since it can sensitize the cancer cell to the conventional treatment. 1. over-expression 2. synthetic lethality partner (which relied on DSB repair) This paper wants to review the suggested "targets" for the enzymes (ending with "ases") in the DSB pw. "TARGETase" 1. Kinases (adding the phosphate group) 2. Phosphatase (removing the phosphate group) 3. Nucleases (cutting the DNA strand at the phospho diester bond) 4. Helicase (unwinding the

Note: p38 inhibitor inhibits the apoptosis of cowanin-treated human colorectal adenocarcinoma cells (doi: 10.3892/ijo.2018.4353) Cowanin is pure cmp. from Garcinia cowa (Chamuay); Crude extract from tree; 1. antitimor activity 2. inflmmation induction 3. antibacterial activity 4. anti-inflammatory activity 5. antimalarial activity Purpose of this study, 1. effects of cowanin on apoptosis induction 2. effect on apoptosis-related protein kinase 3.mitogen-activated protein kinase Target cell line -- LoVo human colorectal cancer cell line Assay test; 1. MTT assay (viability assay) 2. Nuclear morphological change by Hoe staining 3. Mitochondrial membrane potential by JC-1 staining Cowanin inhibits cell proliferation and induced cell dead via apoptosis pw. Cowanin induce all apoptotic related molecules through MAPK and Akt signaling pw. Therefore, the author suggested that cowanin might be a good candidate to treat colorectal cancer. T