Kupfer Lab: Difference between revisions
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[[Kupfer Lab| <font face="trebuchet ms" size="+1" style="color:#ff9900"> '''Home''' </font>]] | |||
[[ | [[Kupfer Lab:Contact | <font face="trebuchet ms" size="+1" style="color:#ff9900"> '''Contact''' </font>]] | ||
[[ | [[Kupfer Lab:Back Door | <font face="trebuchet ms" size="+1" style="color:#ff9900"> '''Internal''' </font>]] | ||
[[ | [[Kupfer Lab:Lab Members | <font face="trebuchet ms" size="+1" style="color:#ff9900"> '''Lab Members''' </font>]] | ||
[[ | [[Kupfer Lab:Reprints | <font face="trebuchet ms" size="+1" style="color:#ff9900"> '''Publications''' </font>]] | ||
[[ | [[Kupfer Lab:Research | <font face="trebuchet ms" size="+1" style="color:#ff9900"> '''Research''' </font>]] | ||
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We have three other ongoing projects related to FA. First, we have begun to purify the protein complexes containing gene products that are defective in 2 additional hematopoietic failure syndromes, Diamond-Blackfan anemia (DBA) and congenital dyserythropoietic anemia (CDA). | =='''Welcome to the Kupfer lab at Yale University'''== | ||
[[Image:Figure1.tiff|thumb|400px|right|'''Fanconi anemia (FA) protein pathway.''' The FA core complex localizes to chromatin during the S phase and in response to DNA damage. Within the core complex, both FANCA and FANCG are phosphorylated (P). In the presence of an intact core complex, FANCD2 is monoubiquitinated (Ub) on K561 and colocalizes in nuclear foci with BRCA1, where it carries out its roles in DNA repair and/or cell cycle control. FANCD2 is a phosphorylation target of kinases ATM and perhaps ATR, a phosphorylation that is necessary to maintain the S-phase checkpoint. At mitosis, FANCG is phosphorylated, and the core complex is excluded from the nucleus and condensed chromatin.]] | |||
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Our lab studies the relationship of genomic instability and the propensity towards development of cancer. Specifically, we focus on the genetic syndrome [http://www.fanconi.org/ Fanconi anemia] (FA). FA serves as a paradigm where the disciplines of development, genetics, and molecular oncology come together. Like other cancer susceptibility syndromes, such as [http://www.atcp.org/ ataxia telangiectasia] and [http://www.xps.org/ xeroderma pigmentosum,]FA patients exhibit a unique hypersensitivity to DNA crosslinking agents, which is the key to the biology of FA. Unlike the other syndromes, exceedingly little is known about FA. To learn more about FA, please visit our [http://openwetware.org/wiki/Kupfer_Lab:Research research link.] | |||
We have three other ongoing projects related to FA. First, we have begun to purify the protein complexes containing gene products that are defective in 2 additional hematopoietic failure syndromes, [http://en.wikipedia.org/wiki/Diamond-Blackfan_anemia/ Diamond-Blackfan anemia (DBA)] and congenital dyserythropoietic anemia (CDA). | |||
Second, we are investigating ways to use our knowledge of genomic instability for improving cancer therapeutics. We have been working on tax1, a viral oncogene, in collaboration with the [http://www.evms.edu/micro/faculty-semmes.html/ Semmes laboratory at Eastern Virginia Medical School]. Interestingly, tax1 chemosensitizes p53 mutant cells in culture. | Second, we are investigating ways to use our knowledge of genomic instability for improving cancer therapeutics. We have been working on tax1, a viral oncogene, in collaboration with the [http://www.evms.edu/micro/faculty-semmes.html/ Semmes laboratory at Eastern Virginia Medical School]. Interestingly, tax1 chemosensitizes p53 mutant cells in culture. | ||
Finally, we have also | Finally, we have also begun a more clinical project, using mass spectroscopy technology to find biomarkers in pediatric cancers. Again in collaboration with the Semmes laboratory, we have adapted the mass spec to analyze sera from patients with Hodgkin disease in order to identify unique protein markers of disease. | ||
== == | |||
'''Who's visiting?''' (got it from [[http://openwetware.org/wiki/Kathleen_McGinness Kathleen]], who thanks [[Barry Canton|Barry]]!) | |||
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Revision as of 21:03, 29 November 2007
Welcome to the Kupfer lab at Yale University
Our lab studies the relationship of genomic instability and the propensity towards development of cancer. Specifically, we focus on the genetic syndrome Fanconi anemia (FA). FA serves as a paradigm where the disciplines of development, genetics, and molecular oncology come together. Like other cancer susceptibility syndromes, such as ataxia telangiectasia and xeroderma pigmentosum,FA patients exhibit a unique hypersensitivity to DNA crosslinking agents, which is the key to the biology of FA. Unlike the other syndromes, exceedingly little is known about FA. To learn more about FA, please visit our research link.
We have three other ongoing projects related to FA. First, we have begun to purify the protein complexes containing gene products that are defective in 2 additional hematopoietic failure syndromes, Diamond-Blackfan anemia (DBA) and congenital dyserythropoietic anemia (CDA).
Second, we are investigating ways to use our knowledge of genomic instability for improving cancer therapeutics. We have been working on tax1, a viral oncogene, in collaboration with the Semmes laboratory at Eastern Virginia Medical School. Interestingly, tax1 chemosensitizes p53 mutant cells in culture.
Finally, we have also begun a more clinical project, using mass spectroscopy technology to find biomarkers in pediatric cancers. Again in collaboration with the Semmes laboratory, we have adapted the mass spec to analyze sera from patients with Hodgkin disease in order to identify unique protein markers of disease.
Who's visiting? (got it from [Kathleen], who thanks Barry!)
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