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So you’ve done the research, gathered up your data into an exciting story, and are ready to present your findings at a conference. But what you get out of a conference depends on what you put into it before, during, and after the meeting. Let’s break it down into the following: the elevator pitch, talks, the poster session, networking, and social media.

Apoptosis or “programmed cell death" plays a pivotal role in an array of biological processes including development, the immune system, and cell turnover. Apoptosis is a highly controlled process that is triggered by internal and external signals such as developmental cues and DNA damage. These signals activate a cascade of caspases, protease enzymes that cleave proteins. Executioner caspases are activated last in the cascade and are responsible for the degradation of over 600 cellular components ultimately leading to cell fragmentation and death (Elmore, 2007).

In 2012, we received the first CRISPR plasmid deposit. Now we have over 8,000 CRISPR plasmids in the repository that have been shared over 140,000 times to over 75 countries. That’s a lot of CRISPR! As we’ve shared these tools over the years, the amount of CRISPR educational resources hosted on our website and blog have grown. We even have a CRISPR eBook. This week, we’ll continue to grow the ways we share science by hosting our first ever CRISPR Week on social media.

Direct reprogramming describes the process where differentiated cells are turned into a cell type of choice while bypassing the intermediate pluripotent state. Though a valuable tool for regenerative medicine, direct reprogramming is an inefficient process, with the majority of cells failing to develop the desired identity.

The development of single cell technologies, such as single cell RNA-seq (scRNA-seq), now allows scientists to identify the gene expression patterns unique to the few cells that successfully reprogram. Unfortunately scRNA-seq only captures the gene expression of cells at a single time point, making it difficult to investigate how early expression patterns influence reprogramming outcomes.

Thousands of mutations have been implicated in cancer. Yet, the majority of them remain uncharacterized. This represents a considerable barrier to furthering research and developing effective treatments for the disease. Recently, Kenneth Scott’s lab at Baylor College of Medicine and Gordon Mills’s lab at the MD Anderson Cancer Center tackled this problem by developing a moderate throughput functional genomic platform to annotate genetic perturbations that may play significant roles in cancer pathogenesis.