SEPTEMBER 2020- NEW! Research Assistant position available immediately!
Our Neurobiology laboratory at UMB is seeking a full-time research technician to carry out mostly biochemical and cell biological bench research activities in the general area of neurodegeneration (Alzheimer’s, Parkinson’s, ALS). The ideal candidate will be a new or recent college graduate (BA or BS in a science-related field is required; grade point should be 3.0 or above) who has significant prior college or summer wet lab research experience. The best fit for this position might be a person taking a year or two off prior to graduate or professional school. This CII contract position offers significant benefits, and a starting salary of at least 39K. The person will be responsible for handling routine laboratory activities (ordering, plasmid purification, cell culture maintenance) but will mostly perform original research activities under the direction of a postdoctoral fellow and/or the lab head. Techniques involved will include, but are likely not limited to, cell culture, immunohistochemistry, protein purification, and spectrophotometric plate assays. We are looking for a helpful, curious, and motivated individual with a deep interest in basic scientific research; note that an opportunity for publication exists. Please see this lab website for further information on laboratory research interests. If your credentials match the above, please send your resume and the names and contact information of two or three references to Dr. Iris Lindberg at ilindberg at som dot umaryland dot edu. UMB is an EE/AA employer.
ALSO: Independent, energetic postdoctoral fellows with research experience in either cell biology and/or biochemistry and an interest in proteostasis and secretory systems are invited to apply to our laboratory. The laboratory is predominantly focused on defining the biological roles of two neuroprotective secretory chaperones specific to neurons with regard to blocking protein aggregation and aggregate propagation in the context of neurodegenerative diseases such as Alzheimer’s and Parkinson’s.
Please email a current CV, a brief statement of your research interests, and the email addresses and phone numbers of three references, to Dr. Iris Lindberg at ilindberg at som dot umaryland dot edu. A recent Ph.D. as well as at least one first-author paper (in a refereed English-language journal) is required. Note that possibility of independent funding is required.
GRADUATE STUDENT ROTATIONS AVAILABLE IMMEDIATELY
We also currently have rotation openings for graduate students, particularly those interested in neurodegeneration. You will learn basic techniques in the molecular and cell biology of neurons, including construction of CRISPR/Cas9 vectors to knock out selected genes, immunofluorescence, and biochemical assays of protein aggregation.
If you would like to rotate in the lab (you must be currently enrolled in a University of Maryland graduate program), please send an email to Iris Lindberg at email@example.com. A minimal eight-week rotation period is required.
Selected Relevant Publications for these two projects:
The neural chaperone proSAAS blocks α-synuclein fibrillation and neurotoxicity.
(2016) Jarvela TS, Lam HA, Helwig M, Lorenzen N, Otzen DE, McLean PJ, Maidment NT, Lindberg I.
Proc Natl Acad Sci U S A. 2016 Aug 9;113(32): PMID:27457957
Chaperones in Neurodegeneration. (2015) Lindberg I, Shorter J, Wiseman RL, Chiti F, Dickey CA, McLean PJ.J Neurosci. 2015 Oct 14;35(41):13853-9.Review. PMID:26468185
A novel function for proSAAS as an amyloid anti-aggregant in Alzheimer’s disease. (2014) Hoshino A, Helwig M, Rezaei S, Berridge C, Eriksen JL, Lindberg I. J Neurochem. 2014 Feb;128(3):419-30. PMID:24102330
The neuroendocrine protein 7B2 suppresses the aggregation of neurodegenerative disease-related proteins. (2013)Helwig M, Hoshino A, Berridge C, Lee SN, Lorenzen N, Otzen DE, Eriksen JL, and Lindberg I. J. Biol. Chem. 11;288(2):1114-24.
Human Obesity SNPs and Mutations
Winters A, Ramos-Molina B, Jarvela TS, Yerges-Armstrong L, Pollin TI, and Lindberg, I. (2017). Diabetes Res Clin Pract. 2017 Jul 3;131:82-90. doi: 10.1016/j.diabres.2017.06.023. [Epub ahead of print]PMID:28719828.
Revisiting PC1/3 mutants: dominant-negative effect of endoplasmic reticulum-retained mutants.
Blanco EH, Ramos-Molina B, Lindberg I.Endocrinology. 2015 J156(10):3625-37. doi: 10.1210/en.2015-1068. Epub 2015 Jul 24.
Defective transport of the obesity mutant PC1/3 N222D contributes to loss of function.
Prabhu, Y., Blanco, E.H., Liu, M., Peinado, J.R., Wheeler, M.C., Gekakis, N., Arvan, P., Lindberg, I.(2014) Endocrinology. Jul;155(7):2391-401.PMID:24828610
Biochemical and cell biological properties of the human prohormone convertase 1/3 Ser357Gly mutation: a PC1/3 hypermorph.
Blanco, EH, Peinado JR, Martín, MG, and Lindberg, I. (2014) Endocrinology. 2014 Sep;155(9):3434-47 PMID:24932808
Congenital proprotein convertase 1/3 deficiency causes malabsorptive diarrhea and other endocrinopathies in a pediatric cohort. (2013) Martín MG, Lindberg I, Solorzano-Vargas RS, Wang J, Avitzur Y, Bandsma R, Sokollik C, Lawrence S, Pickett LA, Chen Z, Egritas O, Dalgic B, Albornoz V, de Ridder L, Hulst J, Gok F, Aydoğan A, Al-Hussaini A, Gok DE, Yourshaw M, Wu SV, Cortina G, Stanford S, Georgia S. Gastroenterology.145(1):138-48. PMID:23562752
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