MODIFICATION
B -- Role of BDNF Receptor TrkB.TI in Cardiomyocytes Function
- Notice Date
- 8/24/2011
- Notice Type
- Modification/Amendment
- NAICS
- 541380
— Testing Laboratories
- Contracting Office
- Department of Health and Human Services, National Institutes of Health, National Cancer Institute, Office of Acquisitions, 6120 Executive Blvd., EPS Suite 600, Rockville, Maryland, 20852
- ZIP Code
- 20852
- Solicitation Number
- NCI-110174-MW
- Archive Date
- 9/23/2011
- Point of Contact
- Melissa R. Ward, Phone: 301-402-4509, Caren N Rasmussen, Phone: (301) 402-4509
- E-Mail Address
-
wardmr@mail.nih.gov, cr214i@nih.gov
(wardmr@mail.nih.gov, cr214i@nih.gov)
- Small Business Set-Aside
- N/A
- Description
- *This notice has been modified to add a twelve month option period. Contracting Office Address Department of Health and Human Services, National Institutes of Health, National Cancer Institute, Office of Acquisitions, 6120 Executive Blvd. EPS Room 6074, Rockville, MD, 20852, UNITED STATES Description The National Cancer Institute (NCI), Center for Cancer Research (CCR), Mouse Cancer Genetics Program (MCGP) plans to procure on a sole source basis the analysis of the role of BDNF Receptor TrkB.Tl in Cardiomyocytes Function from Dr. Gianluca Fulgenzi, Universita Politecnica delle Marche, Polo Murri, Torette di Ancona,Via tronto 10, 60020 Ancona ITALY. The services herein are being procured in accordance with the simplified acquisition procedures as authorized by FAR Part 13.106-1 (b)(1). The North American Industry Classification System code is 541380 and the business size standard is $12.0M. Only one award will be made as a result of this solicitation. This will be awarded as a firm fixed price type contract. Period of Performance shall be twelve (12) months from date of award with one twelve month option period. The neurotrophin receptor TrkB is essential for normal function of the mammalian brain. It is expressed in two major splice variants. Full-length trkB receptors (TrkB.FL) possess an intracellular tyrosine kinase domain and are believed to mediate the crucial effects of brain-derived neurotrophic factor (BDNF). By contrast, truncated receptors TrkB.T1 lack tyrosine kinase activity and have only recently been reported to elicit intracellular signaling. However, the biological significance of this signaling is still completely unknown. Recent studies indicate that TrkB.T1 receptors are expressed in cardiomyocytes without the kinase active receptors providing a suitable system to test the functionality of TrkB.T1 in vivo. In a previous study, investigators at the NCI generated a mouse mutant lacking TrkB.T1 and in the initial characterization found no major abnormalities in cardiac development and function. In a follow-up study, investigators tested whether TrkB.T1 could play a role in stress or pathological conditions; they introduced the TrkB.T1 mutation in the mdx mouse model of muscular dystrophy and found that loss of TrkB.T1 significantly affects the cardiopathy caused by the mdx mutation. This important finding prompted investigation of the molecular mechanisms underlying this effect in vivo by dissecting TrkB.T1 signaling in cardiomyocytes by electrophysiological means; this approach was used because TrkB.T1 activation by BDNF has been reported to cause release of calcium from the cellular intracellular stores. The overall purpose of this project is to dissect TrkB.T1 signaling in cardiomyocytes by electrophysiological means. In the first phase of the project, the contractor shall perform analysis of the heart histological specimens by regular and electron microscopy. Upon completion of the first phase, the contractor shall build a unique instrument that incorporates a photodiode with computer driven shutters and mirrors to measure calcium flux within single cells. Concurrently, the contractor shall develop software applications to collect and analyze data acquired through this photodiode system and record the results. Dr. Gianluca Fulgenzi, is uniquely qualified to perform this work. Dr. Fulgenzi's expertise in electrophysiology, extensive experience with the analysis of the mdx mouse model, and knowledge in cardiomyocytes isolation and biochemistry is not available from any other source; this unique set of skills is key to the success of this project. In addition, Dr. Fulgenzi's expertise in the patch clamp and single cell recording apparatus is invaluable. The technical expertise and "feel" required to use this instrumentation can only be acquired with years of use and experience. The patch clamp system is extremely sensitive and an inexperienced user could easily misinterpret and misconstrue results. This notice is not a request for a competitive quotation. However, if any interested party believes it can meet the above requirement, it may submit a statement of capabilities. The statement of capabilities and any other information furnished must be in writing and must contain material in sufficient detail to allow NCI to determine if the party can perform the requirement. Capability statements must be received in the contracting office by 11:00 AM EST, on September 8, 2011. For further information, please contact Melissa Ward, Contract Specialist via electronic mail at Melissa.Ward@nih.gov. A determination by the Government not to compete this proposed requirement based upon responses to this notice is solely within the discretion of the Government. Information received will be considered solely for the purpose of determining whether to conduct a competitive procurement. No collect calls will be accepted. No faxed or emailed capability statements will be accepted. In order to receive an award, contractors must be registered and have valid certification in the Central Contractor Registration (CCR) and the Online Representations and Certifications Applications (ORCA). Reference: NCI-110174-MW on all correspondence.
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- Record
- SN02547367-W 20110826/110824235807-f3bc40b92e9c7fd2b5f85b0d16be482d (fbodaily.com)
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