SV40 T Antigen Inhibits Expression of MyoD and Myogenin, Up-Regulates Myf-5, but Does Not Affect Early Expression of Desmin or α7 Integrin during Muscle Development

Haider, S.Raza; Wang, Weigwang; Kaufman, Stephen J.

doi:10.1006/excr.1994.1040

Cited by 19 publications

(13 citation statements)

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“…We hypothesized that desmin, which is highly homologous to vimentin, might be affected by NO 2 Tyr depletion of Glu MTs. However, L6 cells were reported not to express desmin (31). Consistent with this finding, we were unable to detect either desmin protein or mRNA on Western or Northern blots, with or without NO 2 Tyr treatment.…”

Section: Lack Of Glu Mts Blocks Expression Of Muscle-specific Structusupporting

confidence: 83%

“…they survived ␤-D-arabinofuranoside treatment) even though they continued to express abundant integrin ␤ 1A . Myogenin up-regulation has been correlated with up-regulation of integrin ␣ 7 (31,44), and lack of myogenin activity in NO 2 Tyrtreated cells (Fig. 4) might contribute to their failure to induce integrin ␣ 7 .…”

Section: Expression Of Cell Adhesion Molecules Is Perturbed By Nomentioning

confidence: 89%

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Alteration of the C-terminal Amino Acid of Tubulin Specifically Inhibits Myogenic Differentiation

Chang¹,

Webster²,

Salam³

et al. 2002

Journal of Biological Chemistry

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Section: Lack Of Glu Mts Blocks Expression Of Muscle-specific Structusupporting

confidence: 83%

Section: Expression Of Cell Adhesion Molecules Is Perturbed By Nomentioning

confidence: 89%

Alteration of the C-terminal Amino Acid of Tubulin Specifically Inhibits Myogenic Differentiation

Chang¹,

Webster²,

Salam³

et al. 2002

Journal of Biological Chemistry

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“…This result could well be related to the inability of SV40 T antigen-immortalized cell lines to undergo late differentiation as recently reported in other models. 26,27 In the present study, we reinvestigated the origin of laminin ␣2 chain following cell transplantation using normal, non-immortalized human myoblasts as well as various mouse myogenic cell lines. The human myoblasts were transplanted into immunodeficient SCID mice to investigate human laminin ␣2 chain expression in vivo.…”

Section: Introductionmentioning

confidence: 99%

Myoblast transplantations lead to the expression of the laminin α2 chain in normal and dystrophic (dy/dy) mouse muscles

et al. 1999

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Laminin-2 is part of the basement membrane of the skelmouse myoblast cell line in dy/dy muscles allows the etal muscle fibers. The laminin ␣2 chain is absent or drastiexpression of the murine laminin ␣2 chain; and (3) allocally reduced in a subgroup of congenital muscular dystransplantation of the D7 dystrophic dy/dy cell line allows trophy patients, and in the severely affected dystrophic the formation of new and hybrid muscle fibers in dy/dy dy/dy mouse. We previously reported that heterogenous muscle in the absence of laminin ␣2 chain expression. We primary mouse muscle cell cultures conferred laminin ␣2 conclude that normal myoblasts are able to restore the chain expression in dy/dy mice muscles upon cell transexpression of an extracellular skeletal muscle protein and plantation. In the present study we investigated whether that the absence of laminin-2 does not prevent transpure myoblast cell lines were able to confer laminin ␣2 planted muscle cells from participating in the formation of chain expression in vivo. We observed that: (1) xenomyofibers. Myoblasts are, therefore, attractive tools for transplantation of non-immortalized human myoblast in further exploration of gene complementation strategies in SCID mouse muscles allows human laminin ␣2 chain the animal models of congenital muscular dystrophy. expression; (2) allotransplantation of the permanent G8

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“…On the other hand several reports indicate that ceils expressing a high amount of desmin but no MyoD and myogenin are incapable of fusion [8,9]. Lack of fusion and absence of functional MyoD and myogenin has often been observed after transfection with oncogenes [10][11][12] or the addition of exogenous growth factors [13,14].…”

Section: Introductionmentioning

confidence: 99%

“…In the case of SV40 large T antigen conflicting results have been reported concerning the inhibitory effect on terminal differentiation [9,20]. Therefore, we have transfected primary hamster muscle cells with a plasmid encoding the large T transcription unit.…”

Section: Introductionmentioning

confidence: 99%

SV40 large T antigen-induced inhibition of terminal differentiation of primary skeletal muscle cells is associated with a block in the expression of MyoD and myogenin

Klundert

Bloemendal

1994

Mol Biol Rep

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Transformation of hamster primary myoblasts with the SV40 large T antigen leads to inhibition of terminal differentiation. This process is associated with a block in the transcription of the muscle-specific determinator genes MyoD and myogenin. The effect of SV40 large T antigen on the terminal differentiation is dominant and cannot be bypassed by re-expression of retrovirally encoded MyoD. The intermediate filament protein desmin is normally up-regulated when myoblasts differentiate into myotubes. Surprisingly, desmin is expressed at relatively high levels in transformed hamster muscle cells grown under proliferative conditions. So desmin expression can be independent of the onset of differentiation. This is in accordance with the expression of the protein in fibroblasts, infected with a MyoD-encoding retrovirus and grown under proliferative conditions, when no other muscle-specific proteins are present.

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SV40 T Antigen Inhibits Expression of MyoD and Myogenin, Up-Regulates Myf-5, but Does Not Affect Early Expression of Desmin or α7 Integrin during Muscle Development

Cited by 19 publications

References 0 publications

Alteration of the C-terminal Amino Acid of Tubulin Specifically Inhibits Myogenic Differentiation

Alteration of the C-terminal Amino Acid of Tubulin Specifically Inhibits Myogenic Differentiation

Myoblast transplantations lead to the expression of the laminin α2 chain in normal and dystrophic (dy/dy) mouse muscles

SV40 large T antigen-induced inhibition of terminal differentiation of primary skeletal muscle cells is associated with a block in the expression of MyoD and myogenin

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