Foundations of Biomedical Sciences Module IV
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MINAR Is a Novel NOTCH-2 Interacting Protein That Regulates NOTCH-2 Activation and Angiogenesis
Boston University OpenBU http://open.bu.edu Theses & Dissertations Boston University Theses & Dissertations 2017 MINAR is a novel NOTCH-2 interacting protein that regulates NOTCH-2 activation and angiogenesis https://hdl.handle.net/2144/23712 Boston University BOSTON UNIVERSITY SCHOOL OF MEDICINE Thesis MINAR IS A NOVEL NOTCH-2 INTERACTING PROTEIN THAT REGULATES NOTCH-2 ACTIVATION AND ANGIOGENESIS by RACHEL XI-YEEN HO B.S., University of Washington, 2015 Submitted in partial fulfillment of the requirements for the degree of Master of Science 2017 © 2017 by RACHEL XI-YEEN HO All rights reserved Approved by First Reader Nader Rahimi, Ph.D. Associate Professor, Department of Pathology & Laboratory Medicine Second Reader Dr Louis C. Gerstenfeld, Ph.D. Professor, Department of Orthopaedic Surgery ACKNOWLEDGEMENTS First, I wish like to thank Dr. Nader Rahimi, whom I look up to as a nurturing mentor and a brilliant scientist. His encouragements and philosophical approach to learning have left a great impression on me and inspired my further development as a scientist. Thank you for giving me the opportunity to study under your guidance and for helping me realize my potential. I would also like to thank all the members from the Rahimi lab, Zou, Rosana, Marwa, Rawan, Tori, Nels, and Esma, whose friendships contributed tremendously to creating a wonderful working environment. Additionally, I thank Dr. Gerstenfeld for his input on my thesis. Finally, I thank my mother and father for their unwavering love and support, and my sister for the late night conversations. This work was supported in part by grants from the NIH (R21CA191970 and R21CA193958 to N.R.) iv MINAR IS A NOVEL NOTCH-2 INTERACTING PROTEIN THAT REGULATES NOTCH-2 ACTIVATION AND ANGIOGENESIS RACHEL XI-YEEN HO ABSTRACT Angiogenesis, the formation of new vessels, is a highly regulated and complex cellular process, which plays a crucial role in physiological processes such as embryological development and wound healing. -
C-Type Lectin CD209L/L-SIGN and CD209/DC-SIGN: Cell Adhesion Molecules Turned to Pathogen Recognition Receptors
biology Review C-type Lectin CD209L/L-SIGN and CD209/DC-SIGN: Cell Adhesion Molecules Turned to Pathogen Recognition Receptors Nader Rahimi Department of Pathology, School of Medicine, Boston University Medical Campus, Boston, MA 02118, USA; [email protected] Simple Summary: COVID-19 pandemic continues to pose a serious threat to global public health with overwhelming worldwide socio-economic disruption. SARS-CoV-2, the viral agent of COVID- 19, uses its surface glycoprotein Spike (S) for host cell attachment and entry. The emerging picture of pathogenesis of SARS-CoV-2 demonstrates that S protein, in addition, to ACE2, interacts with the car- bohydrate recognition domain (CRD) of C-type lectin receptors, CD209L and CD209. Recognition of CD209L and CD209 which are widely expressed in SARS-CoV-2 target organs can facilitate entry and transmission leading to dysregulation of the host immune response and other major organs including, cardiovascular system. Establishing a comprehensive map of the SARS-CoV-2 interaction with CD209 family proteins, and their roles in transmission and pathogenesis can provide new insights into host-pathogen interaction with implications in therapies and vaccine development. Abstract: C-type lectin CD209/DC-SIGN and CD209L/L-SIGN proteins are distinct cell adhesion and pathogen recognition receptors that mediate cellular interactions and recognize a wide range of pathogens, including viruses such as SARS, SARS-CoV-2, bacteria, fungi and parasites. Pathogens exploit CD209 family proteins to promote infection and evade the immune recognition system. CD209L and CD209 are widely expressed in SARS-CoV-2 target organs and can contribute to in- fection and pathogenesis. -
Cell and Molecular Biology Program, You Will Be Expected to Rotate Through Three to Four Laboratories During the Year
Cell and Molecular Biology Program Student Handbook 2010-2011 http://www.bumc.bu.edu/cmbio www.bumc.bu.edu/gms/student-life/gmsso Contents Welcome 3 Organizational Structure 4 Academic Advisors and Student Mentors 5 Information for New Students 6 CMB Monthly Meetings 7 Rotations 8 Dates 8 Presentations 9 Rotation Evaluation Form 10 List of students in program 11 Graduates and where they are now 13 Academic Requirements and Policies 14 Research Training 18 Qualifying examinations 18 Dissertation Advisory Committee 18 Dissertation Defense 21 Pre-thesis committee evaluation forms 22 Mini Courses – Past and Present 23 Faculty that participate in CMB 25 2 Welcome to the Graduate Program The program accepted its first group of students 13 years ago and today 48 students have received their PhDs and entered industry and academia. Ten students in the program have won the coveted Henry I. Russek Achievement award and an even greater number have been awarded second place and honorable mention awards. This is a real honor! We have had 3 students win the Science Competition at the Charles River Campus. In addition, we have had one student participate in the competitive NSF program (K-12) where students teach in local school systems and take courses on learning how to teach. Many have attended local, national and international meetings and given presentations. Most importantly a large number have a great start on their CV with publications. As a member of the program you will be required to take a core set of courses in your first year. At the same time you will be doing research in a number of laboratory rotations in departments that belong to the Program. -
The Role of Shb in Angiogenesis, FGF and VEGF Signalling in Endothelial Cells
Comprehensive Summaries of Uppsala Dissertations from the Faculty of Medicine 1318 The Role of Shb in Angiogenesis, FGF and VEGF Signalling in Endothelial Cells BY KRISTINA HOLMQVIST ACTA UNIVERSITATIS UPSALIENSIS UPPSALA 2004 ! "#$"% & ' ( & & )' ' * & +, -' . / (', 0 1 2, !, -' 3 & 4' 5 ( ( 6 7/6 4( ( / ' , 5 , "#", %% , , 849 :";%%!;%%";# 5 ( ( & ' & & . & ; ( , -' ($ ( & && & ' , 5 ( ( ( & & ( . ' & ' ' ( . ' & *7/6+ & ( . ' & *6+ ' & , 4' 1 . ' ' < , ' & ' & 4' 6; 7/6;( ( ' , 4' . & ' ' 4; ' 6; 7/6; , -' . & ( & ( ;4, ' 4'; ( ( & ' *8/+ . 4; , 6 . 4' 52 .'' . ' ' ' ( & 4', 8/ ( .; 3%2 4' * 40 + 52 ( , -' 40; & 4' . & ""=% ' 7/63; ' ' ( )5/ ( 7/63;, ' & 395 4' < <; . ' 4' ( 52 ( & & 7/6 & 7/63;, 8 4' ' 63;" 7/63; ( ' & 52 ' & & ( .'' & & & . , 8/ . ' 40 & 4' ( & & ' & .' & .; 4' ' ( , - < ( ' ' . ' ' 4' ' ( ( ( ( < ( . ' 52 ( ( ( & & ( , 4' 4 52 5 ( ( 7/63; 63;" / ' 4 ( 4 & & 395 7/6 6 && ( - & 395 ! " #! "$ %&'! ! ()&%'*+ ! > 2 0 1 ! 8449 ;=!= 849 :";%%!;%%";# $ $$$ ;#:!# *' $?? ,<,? @ A $ $$$ ;#:!#+ To myself for being determined and never giving up -
The Ubiquitin-Proteasome System Meets Angiogenesis
Published OnlineFirst February 21, 2012; DOI: 10.1158/1535-7163.MCT-11-0555 Molecular Cancer Review Therapeutics The Ubiquitin-Proteasome System Meets Angiogenesis Nader Rahimi Abstract A strict physiological balance between endogenous proangiogenic and antiangiogenic factors controls endothelial cell functions, such that endothelial cell growth is normally restrained. However, in pathologic angiogenesis, a shift occurs in the balance of regulators, favoring endothelial growth. Much of the control of angiogenic events is instigated through hypoxia-induced VEGF expression. The ubiquitin-proteasome system (UPS) plays a central role in fine-tuning the functions of core proangiogenic proteins, including VEGF, VEGFR- 2, angiogenic signaling proteins (e.g., the PLCg1 and PI3 kinase/AKT pathways), and other non-VEGF angiogenic pathways. The emerging mechanisms by which ubiquitin modification of angiogenic proteins control angiogenesis involve both proteolytic and nonproteolytic functions. Here, I review recent advances that link the UPS to regulation of angiogenesis and highlight the potential therapeutic value of the UPS in angiogenesis-associated diseases. Mol Cancer Ther; 11(3); 538–48. Ó2012 AACR. Introduction tumor mass reaches a macroscopic size, it is becoming Angiogenesis, the growth of new blood vessels from increasingly apparent that angiogenesis is instigated in preexisting vessels, is an important physiological process the early stage of tumor development (5, 7), further sup- in the body that is required for normal wound-healing and porting angiogenesis as a vital component of tumor female reproduction. Pathologic angiogenesis (excessive growth and metastasis. or insufficient) is now recognized as a common denom- VEGF-A also plays a central role in the development of inator underlying a number of deadly and debilitating choroidal neovascularization, and indeed is responsible human diseases, including cancer, age-related macular for both neovascularization and vascular leakage in wet degeneration (AMD), diabetic retinopathy, and cardio- AMD (8). -
Identification of Ligand-Induced Proteolytic Cleavage and Ectodomain Shedding of VEGFR-1/FLT1 in Leukemic Cancer Cells Nader Rahimi,1 Todd E
Published OnlineFirst March 10, 2009; DOI: 10.1158/0008-5472.CAN-08-2905 Published Online First on March 10, 2009 as 10.1158/0008-5472.CAN-08-2905 Research Article Identification of Ligand-Induced Proteolytic Cleavage and Ectodomain Shedding of VEGFR-1/FLT1 in Leukemic Cancer Cells Nader Rahimi,1 Todd E. Golde,2 and Rosana D. Meyer1 1Departments of Pathology and Ophthalmology, Boston University Medical School, Boston, Massachusetts and 2Department of Neuroscience, Mayo Clinic, Mayo Clinic College of Medicine, Jacksonville, Florida Abstract endothelial cells as it is poorly tyrosine phosphorylated (4–7) and Vascular endothelial growth factor receptor-1/fms-related lacks the capacity to induce gene expression (8) or to stimulate tyrosine kinase 1 (VEGFR-1/FLT1)is expressed as a mem- cellular responses such as proliferation and migration in cells with brane-bound receptor tyrosine kinase and as an alternatively endothelial origin (6, 7, 9, 10). spliced soluble protein (sVEGFR-1)containing the 1-6 IgG-like Interestingly, the expression and activation of VEGFR-1 in domain of its ectodomain. sVEGFR-1 is known as a naturally nonendothelial cells, in particular cancer cells, are linked to cell occurring inhibitor of angiogenesis and as a surrogate marker proliferation (11, 12), and a recent study indicates that prevent- for cancer progression; it is also linked to pregnancy-induced ing VEGFR-1 signaling by a VEGFR-1–specific ligand, PlGF-blocking hypertension called preeclampsia and to avascularity of nor- antibody, inhibits tumor growth in mice (13), suggesting a functional mal cornea. It remains an open question whether alternative role for VEGFR-1 signaling in tumor growth. -
June 4, 2015 • St. Louis, Missouri
63RD ASMS CONFERENCE ON MASS SPECTROMETRY AND ALLIED TOPICS May 31 - June 4, 2015 • St. LouiS, Missouri Welcome to the 63rd ASMS Conference on Mass Spectrometry and Allied Topics. Conference program activities and exhibit booths are in America’s Center. Corporate Member hospitality suites are located in the Renaissance Grand Hotel. SPONSORS ASMS gratefully acknowledges the support TABLE OF CONTENTS of these companies. GENERAL INFORMATION ....................................... 2 HOTELS .............................................................. 5 ASMS BOARD OF DIRECTORS ............................ 6 INTEREST GROUPS AND COMMITTEES .................. 7 AWARDS.............................................................. 8 Mobile App and WiFi CONVENTION CENTER FLOOR PLANS ................ 11 CORPORATE HOSPITALITY SUITES ..................... 13 ASMS CORPORATE MEMBERS ......................... 14 Opening Reception PROGRAM ACKNOWLEDGEMENTS ....................... 19 PROGRAM OVERVIEW ........................................ 20 WORKSHOPS ..................................................... 25 Closing Event Titles in the following sections are provided by authors. The complete abstracts are available online: www.asms.org Closing Event The PDF document of proceedings submissions for orals and posters may be viewed online one day after presentation at the conference. CONFERENCE SPONSOR SUNDAY ............................................................ 32 MONDAY ORAL SESSIONS ................................. 32 CONTRIBUTORS TUESDAY ORAL SESSIONS