Sobeck Lab: Difference between revisions
| Line 38: | Line 38: | ||
== Postdoctoral position | ==<span style="color:red">Postdoctoral position available:</span>== | ||
This position will work on elucidating novel functional interactions between FA proteins and ATR/ATM-regulated signaling pathways under normal and perturbed cellular conditions. We are seeking a highly dedicated individual with a solid background in mechanisms of DNA replication and repair, and a strong interest in dissecting the complex DNA damage response mechanisms that protect our cells from mutagenic influences. | This position will work on elucidating novel functional interactions between FA proteins and ATR/ATM-regulated signaling pathways under normal and perturbed cellular conditions. We are seeking a highly dedicated individual with a solid background in mechanisms of DNA replication and repair, and a strong interest in dissecting the complex DNA damage response mechanisms that protect our cells from mutagenic influences. | ||
Please send your CV, contact information of 3 references and a concise statement of your research experience to: | |||
Dr. Alexandra Sobeck, Assistant Professor (asobeck@umn.edu). | |||
Dr. Alexandra Sobeck, Assistant Professor (asobeck@umn.edu) | |||
==<span style="color:blue">!! Mark your calendars for the Fanconi Anemia Research Fund Symposium from September 27-30, 2012 in Denver, Colorado</span>== | ==<span style="color:blue">!! Mark your calendars for the Fanconi Anemia Research Fund Symposium from September 27-30, 2012 in Denver, Colorado</span>== | ||
Revision as of 16:25, 13 June 2012
WELCOME TO THE SOBECK LAB
We are interested in signaling pathways that contribute to the maintenance of genomic stability in our cells and prevent cancer susceptibility in humans. We are studying DNA repair pathways that are activated during the S-phase of the cell cycle when chromosomes replicate.
Our research centers on the Fanconi Anemia (FA) and Breast Cancer associated (BRCA1, BRCA2) repair pathways that are suspected have crucial functions in DNA repair and cell cycle checkpoint activation during S-phase. Humans born with mutations in FA genes have a highly elevated risk to develop certain types of cancers including acute myeloid leukemia (AML) and various types of solid tumors. Acquired mutations and silencing of FA genes have been found in different cancers in the general population and the FA genes are thus considered "caretakers" of our genome. Our goal is to understand the molecular functions of the FA/BRCA proteins (currently 15 FA/BRCA genes are known) and to elucidate how these proteins communicate with other members of the DNA damage response network to control and suppress genomic instability.
Our lab uses a combination of human cell-based assays and extracts prepared from eggs of the African clawed frog, Xenopus laevis. These extracts are naturally cell-cycle synchronized and able to replicate and repair DNA in a test tube, providing us with a cell-free system that can be manipulated in many ways and that allows us to ask specific questions about functions of individual FA/BRCA proteins during the DNA damage response.
In this picture (left to right): Rose Kantor, Charlene Fares, Brittany Feia, Archana Sareen, Jordan Becker, Indrajit Chaudhury, Nicki Adams, Alex Sobeck
Lab News
Postdoctoral position available:
This position will work on elucidating novel functional interactions between FA proteins and ATR/ATM-regulated signaling pathways under normal and perturbed cellular conditions. We are seeking a highly dedicated individual with a solid background in mechanisms of DNA replication and repair, and a strong interest in dissecting the complex DNA damage response mechanisms that protect our cells from mutagenic influences.
Please send your CV, contact information of 3 references and a concise statement of your research experience to: Dr. Alexandra Sobeck, Assistant Professor (asobeck@umn.edu).
!! Mark your calendars for the Fanconi Anemia Research Fund Symposium from September 27-30, 2012 in Denver, Colorado
