Kearney T.W. Gunsalus - PhD Student
[email protected]
Our lab discovered that the transcription factor REST is lost in ~20% of breast cancers; these "RESTless" tumors are particularly aggressive and patients have a very poor disease outcome. I'm looking at genes that are differentially expressed in RESTless and RESTfl tumors. Understanding what makes RESTless tumors so aggressive is the first step towards finding better treatments for patients.
Kassondra Meyer - PhD Student
[email protected]
REST, a transcription factor that is lost in a subset of breast cancer tumors, is an important regulator of many genes. When REST is lost in estrogen receptor positive (ER+) tumors, there is a significantly poorer prognosis in breast cancer patients. I’m comparing the hormonal responses in REST vs. RESTless cells. By studying this difference, we may be able to identify the cellular pathway(s) that are responsible for driving tumor aggression in RESTless tumors.
Barry Schoenike - Associate Researcher and Lab Manager
[email protected]
Barry is involved in every aspect of the lab's function, from detailed analysis of chromatin remodeling complexes to lab management. Currently, his main project focuses on studying transcriptional co-repressors of the transcription factor NRSF (also known as REST). In addition to that project, he assists with almost all of the other projects in the lab. Including noogies (see below).
Allison Kirchner - Undergraduate Student
[email protected]
I am looking at the role of mTOR in neuronal plasticity. mTOR is hyperactive in Tuberous Sclerosis Complex and I am helping the lab figure out how to overcome mTOR overactivation in the brain of TSC mutant mice
On to Pastures New...
Matthew P Wagoner - Ex(!)-PhD Student
[email protected]
Wyatt B. Potter - Ex(!)-PhD Student
[email protected]
Changing strength of neuronal synapses, termed synaptic plasticity, is required for the formation of new memories. We are studying how plasticity in the hippocampus is regulated by glycolysis and metabolic state of neurons. To this end, we combine electrophysiology with biochemistry to characterize the cellular events underlying synaptic potentiation. Metabolic regulation of plasticity has possible therapeutic implications for the treatment of pharmacologically intractable epilepsy.
Ryan Miller-Undegraduate student
rmmiller4@wisc.edu
REST uses a number of corepressors to modify chromatin and repress gene transcription. I'm mapping the suite of corepressors and defining the nature of their interactions so that we can target them therapeutically in cancer and epilepsy.
