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To those who spend countless hours on the lab bench, to those that wake up in the middle of the night to incubate samples, to those that re-run assay after assay, to those that persist through every grant application and peer review, to all who are proud to call themselves scientists, we say thank you.
SALL4 is a zinc finger transcription factor which plays a vital role in maintenance of stem cell identity and stem cell self-renewal through transcriptional repression. It has previously been reported that childhood abuse and neglect compromises neural structure and function which can lead to neurological and psychiatric disorders in adulthood. GlaxoSmithKline's EZH2 team strives to understand the role of EZH2 in cancer biology and to explore how EZH2 inhibitors may have therapeutic benefit in the clinic.
EZH2 is the catalytic subunit of the Polycomb Repressive Complex 2 (PRC2) involved in repression of gene expression through methylation of histone H3 on lysine 27 (H3K27). Send a "tweet" thanking a scientist using #superscientist with a link to their research paper and we'll message you to send you a free Epigentek t-shirt*.
Epigentek is an epigenetics company that specializes in epigenetic kits, antibodies, reagents, and services for epigenetic research in DNA methylation, histone modification, and chromatin studies.
Your research does not go unnnoticed, and neither does your dedication, your passion, your lack of sleep, and your continued efforts to keep doing what you do. This study highlights a new mechanism by which SALL4 represses gene expression through interaction with DNMT’s - a previously unrecognized pathway.
Roth and her team are interested in understanding how environmental factors, such as parenting behavior and social stress, can influence the development of behavior and psychiatric disorders.


Likewise, it has also been shown that early life adversity may affect protein levels of brain-derived neurotrophic factor (BDNF), which is one of several factors mediating neural plasticity.
Activating mutations in EZH2 cause increased H3K27 trimethylation in a subset of diffuse large B-cell lymphomas (DLBCL) and follicular lymphomas. It's because of you and your work that we are closer each day to finding cures, saving lives and making the world better for all of us. Furthermore it proposes that DNA methylation and histone deacetylation mechanisms act synergistically to contribute to the regulatory activities of SALL4.
Using a rodent model of infant maltreatment, this study showed methylation of BDNF DNA through the lifespan to adulthood resulting in reduced BDNF expression in adulthood. The authors have shown that a potent small molecule inhibitor of EZH2 methyltransferase activity, GSK126, is highly selective for EZH2 and effectively inhibits the proliferation of EZH2 mutant DLBCL cell lines and xenografts in mice.
Ad.shRNA-p inhibits Puma expression during thapsigargin-induced ER stress in cardiac myocytes. This study provides new insight into stem cell self-renewal mediated by SALL4 via epigenetic machinery. This condition however, could be rescued by chronic treatment with a DNA methylation inhibitor.
In addition to the potential therapeutic implications for EZH2 mutant lymphoma, GSK126 will also serve as a useful tool to understand the role of EZH2 methyltransferase activity which has previously been unattainable using conventional genetic techniques.


Treatment with the ER stress inducer tunicamycin or thapsigargin did not induce significant apoptosis in the majority of melanoma cell lines, but. Changes in SH-SY5Y cells caused by tunicamycin, probably the second most widely used agent to induce ER stress after thapsigargin, were. They focus on multiple brain regions that play a significant role in behavior and mental health, and that are particularly susceptible to the damaging effects of early-life stress.
Treatment of cells with ER stress inducers such as brefeldin-A or thapsigargin induces the expression of caspase-12 protein and also leads to translocation of cytosolic caspase-7. ER stress induced by thapsigargin treatment activated a signaling pathway that included dephosphorylation of phospho-Ser-473-Akt and activation of.
Using a pharmacologic model that delivered ER stress inducer thapsigargin into the brain, this study demonstrated that a short-term brain ER stress over 3 d was sufficient to. We analyzed their expression levels in Mel-RM and MM200 cells before and after induction of ER stress. Excess glucose (GLUC) or fatty acids (FA) ultimately lead to ?-cell apoptosis by mitochondrial (staurosporine-induced) or ER stress (thapsigargin.




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