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Differential expression of the actin-binding proteins, alpha-actinin-2 and -3, in different species: implications for the evolution of functional redundancy.

Publication: Journal Article

Mills, Yang, Weinberger, Vander Woude, AH Beggs, Easteal, and North. 2001. “Differential Expression of the Actin-Binding Proteins, Alpha-Actinin-2 and -3, in Different Species: Implications for the Evolution of Functional Redundancy.”. Hum Mol Genet 10 (13): 1335-46.

Genotype-phenotype correlation in the long-QT syndrome: gene-specific triggers for life-threatening arrhythmias.

Publication: Journal Article

Schwartz, Priori, Spazzolini, Moss, Vincent, Napolitano, Denjoy, et al. 2001. “Genotype-Phenotype Correlation in the Long-QT Syndrome: Gene-Specific Triggers for Life-Threatening Arrhythmias.”. Circulation 103 (1): 89-95.

Human neuropilin-1 and neuropilin-2 map to 10p12 and 2q34, respectively.

Publication: Journal Article

Rossignol, AH Beggs, Pierce, and Klagsbrun. 1999. “Human Neuropilin-1 and Neuropilin-2 Map to 10p12 and 2q34, Respectively.”. Genomics 57 (3): 459-60.

alpha-actinin-2 is a new component of the dystrophin-glycoprotein complex.

Publication: Journal Article

Hance, Fu, Watkins, AH Beggs, and Michalak. 1999. “Alpha-Actinin-2 Is a New Component of the Dystrophin-Glycoprotein Complex.”. Arch Biochem Biophys 365 (2): 216-22.

Molecular genetics of long-QT syndrome.

Publication: Journal Article

Wattanasirichaigoon, and AH Beggs. 1998. “Molecular Genetics of Long-QT Syndrome.”. Curr Opin Pediatr 10 (6): 628-34.

51st ENMC International Workshop: Nemaline Myopathy. 13-15 June 1997, Naarden, The Netherlands.

Publication: Journal Article

Wallgren-Pettersson, AH Beggs, and Laing. 1998. “51st ENMC International Workshop: Nemaline Myopathy. 13-15 June 1997, Naarden, The Netherlands.”. Neuromuscul Disord 8 (1): 53-6.

A severe muscular dystrophy patient with an internally deleted very short (110 kD) dystrophin: presence of the binding site for dystrophin-associated glycoprotein (DAG) may not be enough for physiological function of dystrophin.

Publication: Journal Article

Arikawa-Hirasawa, Koga, Tsukahara, Nonaka, Mitsudome, Goto, AH Beggs, and Arahata. 1995. “A Severe Muscular Dystrophy Patient With an Internally Deleted Very Short (110 KD) Dystrophin: Presence of the Binding Site for Dystrophin-Associated Glycoprotein (DAG) May Not Be Enough for Physiological Function of Dystrophin.”. Neuromuscul Disord 5 (5): 429-38.

ELISA quantitation of dystrophin for the diagnosis of Duchenne and Becker muscular dystrophies.

Publication: Journal Article

Byers, Neumann, AH Beggs, and Kunkel. 1992. “ELISA Quantitation of Dystrophin for the Diagnosis of Duchenne and Becker Muscular Dystrophies.”. Neurology 42 (3 Pt 1): 570-6.

Detection of 98% of DMD/BMD gene deletions by polymerase chain reaction.

Publication: Journal Article

Beggs, AH, Koenig, Boyce, and Kunkel. 1990. “Detection of 98% of DMD/BMD Gene Deletions by Polymerase Chain Reaction.”. Hum Genet 86 (1): 45-8.

Enormous dystrophin in a patient with Becker muscular dystrophy.

Publication: Journal Article

Angelini, AH Beggs, Hoffman, Fanin, and Kunkel. 1990. “Enormous Dystrophin in a Patient With Becker Muscular Dystrophy.”. Neurology 40 (5): 808-12.