Ahmad M. Khalil, PhD, knew the odds were against him — as in thousands upon thousands to one. Yet he More »
Scientists develop a novel method to suppress malaria parasite’s virulence genes, break the code of its immune evasion
Revealed: how malaria evades the immune response by using long noncoding RNA to express one gene while silencing others Up More »
Long non-coding RNAs (lncRNAs) are emerging as important regulatory molecules in developmental, physiological, and pathological processes. However, the precise mechanism More »
Highly motivated postdoctoral candidates are invited to lead several new projects to address fundamental questions in Biology. Current directions in the lab include nucleic acid interactions with proteins and small molecules, and microRNA biology.
The Johns Hopkins Medical Institutions provide a stimulating and collaborative environment for biomedical research. Our lab is affiliated with the Department of Biochemistry and Molecular Biology of the Bloomberg School of Public Health and the Department of Neuroscience of the School of Medicine. The Baltimore/Washington D.C. area also offers rich professional and living opportunities.
Candidates should have a doctoral degree and strong research background. Please send a statement of research experience and career goals, a copy of Curriculum Vitae, and contact information of at least one reference to Dr. Jiou Wang at firstname.lastname@example.org.
More information available at: http://www.jhsph.edu/faculty/directory/profile/5049/Wang/Jiou. The Johns Hopkins University is an Equal Opportunity Employer.
Ahmad M. Khalil, PhD, knew the odds were against him — as in thousands upon thousands to one.
Yet he and his team never wavered from their quest to identify the parts of the body responsible for revving up one of the most aggressive forms of breast cancer, HER2+. This month in Breast Cancer Research and Treatment, Khalil and his colleagues at Case Western Reserve University proved the power of persistence; from a pool of more than 30,000 possibilities, they found 38 genes and molecules that most likely trigger HER2+ cancer cells to spread.
By narrowing what was once an overwhelming range of potential culprits to a relatively manageable number, Khalil and his team dramatically increased the chances of identifying successful treatment approaches to this particularly pernicious form of breast cancer. The HER2+ subtype accounts for approximately 20 to 30 percent of early-stage breast cancer diagnoses, which are estimated to be more than 200,000 new breast cancer diagnoses each year in this country, leading to approximately 40,000 deaths annually. Several cancer chemotherapy drugs do work well at early stages of the disease — destroying 95 to 98 percent of the cancer cells in HER2+ tumors.
Long non-coding RNAs (lncRNAs) regulate diverse biological processes, including cell lineage specification. Here, researchers from Harvard Medical School report transcriptome profiling of human endoderm and pancreatic cell lineages using purified cell populations. Analysis of the data sets allows us to identify hundreds of lncRNAs that exhibit differentiation-stage-specific expression patterns. As a first step in characterizing these lncRNAs, they focus on an endoderm-specific lncRNA, definitive endoderm-associated lncRNA1 (DEANR1), and demonstrate that it plays an important role in human endoderm differentiation. DEANR1 contributes to endoderm differentiation by positively regulating expression of the endoderm factor FOXA2. Importantly, overexpression of FOXA2 is able to rescue endoderm differentiation defects caused by DEANR1 depletion. Mechanistically, DEANR1 facilitates FOXA2 activation by facilitating SMAD2/3 recruitment to the FOXA2 promoter. Thus, this study not only reveals a large set of differentiation-stage-specific lncRNAs but also characterizes a functional lncRNA that is important for endoderm differentiation.
- Jiang W, Liu Y, Liu R, Zhang K, Zhang Y. (2015) The lncRNA DEANR1 Facilitates Human Endoderm Differentiation by Activating FOXA2 Expression. Cell Rep [Epub ahead of print]. [article]
These clips are highlights taken from some iPlant session presentations at the International Plant and Animal Genome Meeting XXIII (January 2015, San Diego). iPlant users from across the US presented on how they have leveraged various iPlant resources to enable their research and educational goals. Importantly, everything they have done, you can do using iPlant. To learn more about the individual projects presented in these clips, see details at www.iplantc.org/pag2015. For your own free iPlant account, and to learn how to do more with iPlant, visit our homepage – www.iplantc.org
BOSTON — Pseudogenes, a sub-class of long non-coding RNA (lncRNA) that developed from the genome’s 20,000 protein-coding genes but lost the ability to produce proteins, have long been considered nothing more than genomic “junk.” Yet the retention of these 20,000 mysterious remnants during evolution has suggested that they may in fact possess biological functions and contribute to the development of disease.
Now, a team led by investigators in the Cancer Research Institute at Beth Israel Deaconess Medical Center (BIDMC) has provided some of the first evidence that one of these non-coding “evolutionary relics” actually has a role in causing cancer. In a new study in the journal Cell, publishing online today, the scientists report that independent of any other mutations, abnormal amounts of the BRAF pseudogene led to the development of an aggressive lymphoma-like disease in a mouse model, a discovery that suggests that pseudogenes may play a primary role in a variety of diseases. Importantly, the new discovery also suggests that with the addition of this vast “dark matter” the functional genome could be tremendously larger than previously thought – triple or quadruple its current known size.