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European Journal of Clinical Pharmacology|January 1, 1984
Assessment of adverse drug reactions in psychiatric hospitalsR Grohmann, H Hippius, B Müller-Oerlinghausen, et al.
Human Molecular Genetics|May 1, 1997
Profound biotinidase deficiency caused by a point mutation that creates a downstream cryptic 3' splice acceptor site within an exon of the human biotinidase geneR J Pomponio, T R Reynolds, H Mandel, et al.
Alzheimer'S Research & Therapy|September 4, 2013
Apolipoprotein E as a β-amyloid-independent factor in Alzheimer's diseaseAndrew B Wolf, Jon Valla, Guojun Bu, et al.
Pediatric Research|December 13, 1997
Mutations in the human biotinidase gene that cause profound biotinidase deficiency in symptomatic children: molecular, biochemical, and clinical analysisR J Pomponio, J Hymes, T R Reynolds, et al.
Multiple Sclerosis and Related Disorders|September 23, 2019
Rituximab-induced serum sickness in multiple sclerosis patientsAndrew B Wolf, Lana Zhovtis Ryerson, Krupa Pandey, et al.
Cell Death and Differentiation|April 25, 2000
Bcl-xL does not inhibit the function of Apaf-1D D Newmeyer, E Bossy-Wetzel, R M Kluck, et al.
Evolution; International Journal of Organic Evolution|November 17, 2007
Genetic variation in pleiotropy: differential epistasis as a source of variation in the allometric relationship between long bone lengths and body weightMihaela Pavlicev, Jane P Kenney-Hunt, Elizabeth A Norgard, et al.
American Journal of Ophthalmology|April 15, 1991
Variable expression of albinism within a single kindredS Castronuovo, J W Simon, G L Kandel, et al.
Cell|April 10, 1987
Regulation of the human interleukin-2 receptor alpha chain promoter: activation of a nonfunctional promoter by the transactivator gene of HTLV-IS L Cross, M B Feinberg, J B Wolf, et al.
Biochemical and Molecular Medicine|June 1, 1997
Mutation (Q456H) is the most common cause of profound biotinidase deficiency in children ascertained by newborn screening in the United StatesK J Norrgard, R J Pomponio, K L Swango, et al.
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