Random Records

It is very old paper though - Note for: Reduced X-Ray Resistance and Homologous Recombination Frequencies in a RAD54 (-/-) Mutant of the Chicken DT40 Cell Line (doi: 10.1016/S0092-8674(00)80198-1 ) Done in S. cerevisiae before and want to investigate in vertebrate -- therefore, DT40 is chosen. 1. Rad54(-/-) was generated 2. Testing this KO - found out that sensitive to radiation, Ig gene conversion reduce, lower targeted integration 3. Complementary testing with human cDNA -- regain radio-resistant and targeted integration **first report on DBS in vertebrate cells. In yeast model study --> found out that either Rad51,Rad52 and Rad54 mutants --> DSB stay long after injure by X-ray Targeted integration in mammal is hard due to the majority of DSB repair occurs through NHEJ (my guess would be less S-phase period and no check point during intra-S? --> need to check which mammalian cell lines were used) Vertebrate cell line model: DT40 is a good mode

Note for: The DNA-damage response in human biology and disease (doi: 10.1038/nature08467) DNA damage response detection is very essential process in living organism to maintain the right balance between the diversity (fit well to the external) and the disease (unfit to the external). 1.DNA lesion can occur either both physiological and pathological condition. 2.physilogical lesion -- DNA mismatch//break by topo-i and topo-ii Damage occurs through: 1.oxidative respiration 2.redox-cycling (membrane of mitochondria) 3.Fenton reaction (redox reaction catalyzed by Fe) 4.NOS and ROS produce during inflammation and infection DNA double-strand break is rarely found but very toxic once it is generated. DNA damage responses differentially occur depending on the classes of DNA lesions. The process could be separated as follow; 1.damage or stalled replication/transcription 2.detection by sensors 3.recruitment of mediators 4.amplifying the signal 5.transduc

Note for: Molecular Role of RNF43 in Canonical and Noncanonical Wnt Signaling (doi: 10.1128/MCB.00159-15) It is a bit hard to follow when reading this paper. Wnt1 class-- canonical Wnt go through beta-catenin Degradation complex includes; 1.adenomatous polyposis coli (APC) 2.axin 3.casein kinase Ialpha (CKIalpha) 4.glycogen synthase kinase 3beta (GSK-3beta) No Wnt-stimulant --> beta catenin is phosphorylated by degradation cpx leading to degradation by ubiquitin proteasome system by interact through SCFbetaTrCP ubiquitin ligase Finalized Wnt-catenin activation --> produce c-Myc which maintains undifferentiated state of cells. Wnt5a class-- non-canonical Wnt 1.not cause accumulation of beta-catenin and no induction of target genes 2.involve in cell polarity and cell migration+antagonizes Wnt/beta-catenin -- play role as tumor suppressor RNF43 suppresses both canonical and non-canonical but in different manner -- The research quest

Paper: Genetics of Opisthorchis viverrini-related cholangiocarcinoma (doi: 10.1097/MOG.0000000000000162) Aim: Looking at the genetic, epigenetic, and transcriptional landscape of CCA Method; whole exome sequencing and target sequencing Finding; CCA-related genes mutations TP53 KRAS SMAD4 novel CCA-related genes mutations chromatin remodeling BAP1 ARID1A MLL3 IDH1/2 Wnt-signaling RNF43 PEG3 KRAS/G-protein GNAS ROBO2 OV and non-OV related; Set of gene mutations  are different which may link to different pathogenesis of CCA Adult Ov can stay at the biliary tract and remain in host for 10 years Important risk factor for CCA; Chronic inflammation in biliary tract epithelia Epigenetic changes for Ov-related; Hypermethylation of hMLH1 promoter (44.6%) -- reduced expression  and function (to me no surprised why it affect the RNF43 mutations -- due to RNF43 has the microsatellite in the coding region which is prone to miss