This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Multiple Endocrine Neoplasia Type (MEN) is an automsomal dominant malignancy that is characterized by tumors of endocrine tissues. The genetic mechanism responsible for this malignancy has been linked to mutations of the Menin tumor suppressor. Despite the wealth of genetic data that support Menin?s role in MEN1 disease, the biochemical function of Menin is still unknown. However, recent studies have demonstrated that the tumor suppressor function of Menin resides in its ability to repress the transcriptional activity of a number of growth-promoting transcription factors, including JunD, Smad3 and

Agency
National Institute of Health (NIH)
Institute
National Center for Research Resources (NCRR)
Type
Biotechnology Resource Grants (P41)
Project #
3P41RR015301-05S1
Application #
7369483
Study Section
Special Emphasis Panel (ZRG1)
Project Start
2005-06-01
Project End
2007-05-31
Budget Start
2005-06-01
Budget End
2007-05-31
Support Year
5
Fiscal Year
2006
Total Cost
$1,837
Indirect Cost
Name
Cornell University
Department
Chemistry
Type
Schools of Arts and Sciences
DUNS #
872612445
City
Ithaca
State
NY
Country
United States
Zip Code
14850
Chen, Wenyang; Mandali, Sridhar; Hancock, Stephen P et al. (2018) Multiple serine transposase dimers assemble the transposon-end synaptic complex during IS607-family transposition. Elife 7:
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