Modulation of microfilament protein composition by transfected cytoskeletal actin genes. | Zendy

S Y Ng | Zendy; Harry P. Erba | Zendy; Gerald Latter | Zendy; Larry Kedes | Zendy; John Leavitt | Zendy

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Modulation of microfilament protein composition by transfected cytoskeletal actin genes.

Author(s) -

S Y Ng,

Harry P. Erba,

Gerald Latter,

Larry Kedes,

John Leavitt

Publication year - 1988

Publication title -

molecular and cellular biology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.14

H-Index - 327

eISSN - 1067-8824

pISSN - 0270-7306

DOI - 10.1128/mcb.8.4.1790

Subject(s) - biology , actin , transfection , microfilament , microbiology and biotechnology , actin binding protein , actin remodeling , gene isoform , cytoskeleton , tropomyosin , actin remodeling of neurons , beta (programming language) , gene , actin cytoskeleton , cell , biochemistry , computer science , programming language

HuT-14T is a highly tumorigenic fibroblast cell line which exhibits a reduced steady-state level of beta-actin due to coding mutations in one of two beta-actin alleles. The normal rate of total actin synthesis could be restored in some clones of cells following transfection of the functional beta-actin gene but not following transfection of the functional gamma-actin gene. In gamma-actin gene-transfected substrains that have increased rates of gamma-actin synthesis, beta-actin synthesis is further reduced in a manner consistent with an autoregulatory mechanism, resulting in abnormal ratios of actin isoforms. Thus, both beta- and gamma-actin proteins can apparently regulate the synthesis of their coexpressed isoforms. In addition, decreased synthesis of normal beta-actin seems to correlate with a concomitant down-regulation of tropomyosin isoforms.

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