Category Biology/Biotechnology

Unexpected Role for Epigenetic Enzymes in Cancer

KDM5s are involved in selection of polyA sites. (A) Western blot and (B) RT-qPCR analyses of MCF7 cells treated with dimethyl sulfoxide (DMSO) or 10 μM KDM5-C70 for 3 days. The ratio of 3′UTR to CDS for CCND1 mRNA was plotted. Error bars represent SEM for biological triplicate experiments. (C) Western blot and (D) RT-qPCR analyses of HeLa cells treated with DMSO or 10 μM KDM5-C70 for 3 days. The ratio of 3′UTR to CDS for DICER1 mRNA was plotted. Error bars represent SEM for biological triplicate experiments. **P < 0.01. (E) RT-qPCR analysis of HeLa/iCas9-c1 cells transduced with lentiviruses carrying single-guide RNAs against KDM5A, KDM5B, KDM5C, or nontargeting control. The ratio of 3′UTR to CDS for DICER1 mRNA was plotted. KO, knockout. Error bars represent SEM for biological triplicate experiments. *P < 0.05; **P < 0.01. (F) Working model for KDM5 involvement in APA. KDM5 recruits the polyA machinery to nascent RNA to modulate polyA site choices. Demethylation or hydroxylation of certain subunits of the polyA machinery by KDM5 also contributes to selection of the polyA sites. The polyA sites (dashes) are noted on the nascent transcript.

KDM5s are involved in selection of polyA sites. (A) Western blot and (B) RT-qPCR analyses of MCF7 cells treated with dimethyl sulfoxide (DMSO) or 10 μM KDM5-C70 for 3 days. The ratio of 3′UTR to CDS for CCND1 mRNA was plotted. Error bars represent SEM for biological triplicate experiments. (C) Western blot and (D) RT-qPCR analyses of HeLa cells treated with DMSO or 10 μM KDM5-C70 for 3 days. The ratio of 3′UTR to CDS for DICER1 mRNA was plotted. Error bars represent SEM for biological triplicate experiments. **P < 0.01. (E) RT-qPCR analysis of HeLa/iCas9-c1 cells transduced with lentiviruses carrying single-guide RNAs against KDM5A, KDM5B, KDM5C, or nontargeting control. The ratio of 3′UTR to CDS for DICER1 mRNA was plotted. KO, knockout...

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Using Fat to help Wounds Heal Without Scars

This is a comparison of wounds healing with and without hair follicles. Credit: Penn Medicine

This is a comparison of wounds healing with and without hair follicles. Credit: Penn Medicine

Breaking ground on method to transform cells. Doctors have found a way to manipulate wounds to heal as regenerated skin rather than scar tissue. The method involves transforming the most common type of cells found in wounds into fat cells – something that was previously thought to be impossible in humans. Researchers began this work at the Perelman School of Medicine at the University of Pennsylvania, which led to a large-scale, multi-year study in connection with the Plikus Laboratory for Developmental and Regenerative Biology at the University of California, Irvine.

Fat cells, ie adipocytes are normally found in the skin, but they’re lost when wounds heal as scars...

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Artificial Leaf goes more Efficient for Hydrogen generation

This is the newly-developed hetero-type dual photoelectrodes by Professor Jae Sung Lee and Professor Ji-Wook Jang's joint reserach team. Credit: UNIST

This is the newly-developed hetero-type dual photoelectrodes by Professor Jae Sung Lee and Professor Ji-Wook Jang’s joint reserach team. Credit: UNIST

An international team with UNIST has engineered a new artificial leaf that can convert sunlight into fuel with groundbreaking efficiency. In the study, the research presented a hetero-type dual photoelectrodes, in which 2 photoanodes of different bandgaps are connected in parallel for extended light harvesting. Their new artificial leaf mimics the natural process of underwater photosynthesis of aquatic plants to split water into hydrogen and oxygen, which can be harvested for fuel.

This study is expected to contribute greatly to the reduction and treatment of carbon dioxide emissions in accordance with the recent Paris Agreement on climate c...

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Promising new Drug stops spread of Melanoma by 90%

Melanoma

Melanoma metastases

Michigan State University researchers have discovered that a chemical compound, and potential new drug, reduces the spread of melanoma cells by up to 90%. The human-made, small-molecule drug compound goes after a gene’s ability to produce RNA molecules and certain proteins in melanoma tumors. This gene activity, or transcription process, causes the disease to spread but the compound can shut it down. Up until now, few other compounds of this kind have been able to accomplish this.

“It’s been a challenge developing small-molecule drugs that can block this gene activity that works as a signaling mechanism known to be important in melanoma progression,” said Richard Neubig, a pharmacology professor...

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