Appearance of acetylcholinesterase molecular forms in noninnervated cultured primary chick muscle cells

1983 ◽  
Vol 3 (3) ◽  
pp. 263-277 ◽  
Author(s):  
Heinz Popiela ◽  
Robert L. Beach ◽  
Barry W. Festoff
Keyword(s):  
Muscle Cells ◽  
Molecular Forms ◽  
Acetylcholinesterase Molecular Forms

Acetylcholinesterase molecular forms in muscle and non-muscle cells of rat heart

1989 ◽  
Vol 21 (10) ◽  
pp. 987-994 ◽  
Author(s):  
Cynthia Nyquist-Battie ◽  
Russel T. Dowell ◽  
Hugo Fernandez
Keyword(s):  
Rat Heart ◽  
Muscle Cells ◽  
Molecular Forms ◽  
Acetylcholinesterase Molecular Forms

Preferential inhibition of acetylcholinesterase molecular forms in rat brain

1992 ◽  
Vol 17 (5) ◽  
pp. 489-495 ◽  
Author(s):  
Nobuo Ogane ◽  
Ezio Giacobini ◽  
Erik Messamore
Keyword(s):  
Rat Brain ◽  
Molecular Forms ◽  
Acetylcholinesterase Molecular Forms

scholarly journals Expression of conventional and novel glucose transporters, GLUT1, -9, -10, and -12, in vascular smooth muscle cells

2013 ◽  
Vol 304 (6) ◽  
pp. C574-C589 ◽  
Author(s):  
Rajkumar Pyla ◽  
Ninu Poulose ◽  
John Y. Jun ◽  
Lakshman Segar
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Relative Abundance ◽  
Glucose Transporters ◽  
Muscle Cells ◽  
Molecular Forms ◽  
Pcr Analysis ◽  
Glut1 Protein

Intimal hyperplasia is characterized by exaggerated proliferation of vascular smooth muscle cells (VSMCs). Enhanced VSMC growth is dependent on increased glucose uptake and metabolism. Facilitative glucose transporters (GLUTs) are comprised of conventional GLUT isoforms (GLUT1–5) and novel GLUT isoforms (GLUT6–14). Previous studies demonstrate that GLUT1 overexpression or GLUT10 downregulation contribute to phenotypic changes in VSMCs. To date, the expression profile of all 14 GLUT isoforms has not been fully examined in VSMCs. Using the proliferative and differentiated phenotypes of human aortic VSMCs, the present study has determined the relative abundance of GLUT1–14 mRNAs by quantitative real-time PCR analysis. Twelve GLUT mRNAs excluding GLUT7 and GLUT14 were detectable in VSMCs. In the proliferative phenotype, the relative abundance of key GLUT mRNAs was GLUT1 (∼43%) > GLUT10 (∼26%) > GLUT9 (∼13%) > GLUT12 (∼4%), whereas in the differentiated phenotype the relative abundance was GLUT10 (∼28%) > GLUT1 (∼25%) > GLUT12 (∼20%) > GLUT9 (∼14%), together constituting 86–87% of total GLUT transcripts. To confirm the expression of key GLUT proteins, immunoblot and immunocytochemical analyses were performed using GLUT isoform-specific primary antibodies. The protein bands characteristic of GLUT1, -9, -10, and -12 were detected in VSMCs in parallel with respective positive controls. In particular, GLUT1 protein expression showed different molecular forms representative of altered glycosylation. While GLUT1 protein displayed a predominant distribution in the plasma membrane, GLUT9, -10, and -12 proteins were mostly distributed in the intracellular compartments. The present study provides the first direct evidence for GLUT9 and GLUT12 expression in VSMCs in conjunction with the previously identified GLUT1 and GLUT10.

Expression of adult fast pattern of acetylcholinesterase molecular forms by mouse satellite cells in culture

1987 ◽  
Vol 36 (3) ◽  
pp. 194-198 ◽  
Author(s):  
M. Immacolata Senni ◽  
Francesco Castrignanò ◽  
Giancarlo Poiana ◽  
Giulio Cossu ◽  
Gianfranco Scarsella ◽  
...  
Keyword(s):  
Satellite Cells ◽  
Molecular Forms ◽  
Cells In Culture ◽  
Acetylcholinesterase Molecular Forms
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