Random Records

Note: Dynamic behavior of DNA topoisomerase IIbeta in response to DNA double-strand breaks (doi: 10.1038/s41598-018-28690-6) DNA topoisomerase II (Topo II) -plays important roles in various cellular processes, such as replication, transcription, and chromosome segregation. DNA topology problems may also occur during DNA repair, the possible involvement of Topo II in this process remains to be fully investigated. rapid recruitment of EGFP-tagged Topo IIβ to the DSB site. Topo IIβ is highly mobile in the nucleus. The Topo II catalytic inhibitors ICRF-187 and ICRF-193 reduced the Topo IIβ mobility and thereby prevented Topo IIβ recruitment to DSBs. Furthermore, Topo IIβ knockout cells exhibited increased sensitivity to bleomycin and decreased DSB repair mediated by homologous recombination (HR), implicating the role of Topo Iiβ in HR-mediated DSB repair. DNA topoisomerase II (Topo II) is an ATP-dependent enzyme that resolves DNA topological problems, such as superco

Note: The Unusual Case of Porcupine (doi:10.1126/science.1228179) Forward chemical genetics: Know the target of the chemical compound -- screening for the phenotype in cells Reverse chemical genetics: Know the protein target -- screening for the action of the chemical compound Wnt proteins is pivotal in animal development and tissue homeostasis, and has become a high-priority anticancer drug target given its essential role in colorectal cancer and its contribution to a broad range of other cancer types. Roel Nusse, Varmus linked deviant activity of Wnt molecules to cancer. LGK974—an acyltransferase called Porcupine (Porcn) that adds fatty acid to Wnt—has been well studied, few of the meeting participants were aware of the drug candidate. Discovered in screens for genes that affect embryonic patterning in the fruit fly, PORCN is the founding member of a 16-gene family with predicted acyltransferase activity. The fatty acyl modification of Wnt, Hedgehog, and

I am not the signaling person but very curious to know how many cellular signaling do the cells have? Not so sure, every cell has all these pathways -- probably not I think..., -- Each pathway might have some molecules which interplays between the signal to response toward the stimuli (growth, stress, chemical, infection, etc.) correctly. 1.Akt Signaling Pathway 2.AMPK Signaling Pathway 3.Apoptosis Signaling Pathway 4.Estrogen Signaling Pathway 5.Insulin Signaling Pathway 6.JAK-STAT Signaling Pathway 7.MAPK Signaling Pathway 8.mTOR Signaling Pathway 9.NF-κB Signaling Pathway 10.Notch Signaling Pathway 11.p53 Signaling Pathway 12.TGF-β Signaling Pathway 13.Toll-like Receptor Signaling Pathway 14.VEGF Signaling Pathway 15.Wnt Signaling Pathway Ref: h ttps://www.tocris.com/signaling-pathways#.WD6R8FyoN0w

Note for: DNA double-strand break repair pathway choice: a chromatin based decision? (doi: 10.1080/19491034.2015.1010946) The choice between these pathways is a critical, yet not completely understood, aspect of DSB repair. DSBs induced across the genome are not repaired by the same pathway. DSBs induced in active genes, naturally enriched in the trimethyl form of histone H3 lysine 36 (H3K36me3), are channeled to repair by HR, in a manner depending on SETD2, the major H3K36 trimethyltransferase. This “decision making” function of preexisting chromatin structure in DSB repair could connect the repair pathway used to the type and function of the damaged region, not only contributing to genome stability but also to its diversity. Importantly failure or misuse of each of these DSB repair pathways can trigger very different consequences on the genome. NHEJ is the primary cause of translocations and dysfunctional telomeres fusion. HR pathways can be entirely conservative when the

Note: Endogenous DNA Double-Strand Breaks during DNA Transactions: Emerging Insights and Methods for Genome-Wide Profiling (doi: 10.3390/genes9120632) Additionally, chromatin looping involved in 3D genome organization and gene regulation is increasingly recognized as a possible contributor to DSB events. This review; 1.mechanisms of endogenous DSB formation 2.genome-wide profiling of DSB Future direction on this field -- genome-wide DSB formation and repair. DSBs can trigger cell death or give rise to structural genomic rearrangements associated with carcinogenesis and other diseases. The frequency of DSBs is estimated to be 10–50 events per cell per day. in healthy individuals the majority of DSBs is thought to originate from within the nucleus, where DSBs form during fundamental processes such as DNA replication, meiosis, antibody diversification, gene transcription, and—although indirectly—cellular metabolism. DNA transactions—especially during DNA rep