c-Myb-binding Sites Mediate G1/S-associated Repression of the Plasma Membrane Ca2+-ATPase-1 Promoter

Afroze, Talat; Husain, Mansoor

doi:10.1074/jbc.275.12.9062

Cited by 38 publications

(26 citation statements)

References 66 publications

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“…Every coin has two sides, and the transcription factor MYB, also known as a proto-oncogene, operates as a transcriptional activator as well as transcriptional repressor. [30][31][32][33] Hitherto, some evidence has strengthened the case that MYB can transactivate Bcl-2 by recognizing the transcription factor binding site (TFBS). 34,35 More excitingly, the data from our study revealed that MYB functions as a transcriptional repressor by inhibiting miR-148a, which could also silence Bcl-2.…”

Section: Discussionmentioning

confidence: 99%

MiR-148a promotes apoptosis by targeting Bcl-2 in colorectal cancer

et al. 2011

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Section: Discussionmentioning

confidence: 99%

MiR-148a promotes apoptosis by targeting Bcl-2 in colorectal cancer

et al. 2011

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“…Both c-Myb and calcineurin influence Ca 2ϩ -mediated signals of cell cycle (1,22,47,48 influx and a c-Myb-dependent reduction in Ca 2ϩ efflux mediated via repression of PMCA1 (1,22,23,40,41). Indeed, ϳ60% of the c-Myb effect on VSMC proliferation is exerted via PMCA1 repression (22).…”

Section: Discussionmentioning

confidence: 99%

“…We previously showed that the cell cycle-associated repression of PMCA1 expression during G 0 to G 1 /S progression in rat VSMC is mediated by the c-Myb transcription factor (1). However, the mechanism(s) underlying the cell cycle-associated repression of PMCA4 had not been elucidated.…”

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confidence: 99%

Calcineurin-independent regulation of plasma membrane Ca²⁺ ATPase-4 in the vascular smooth muscle cell cycle

Afroze

Yang

Wang

et al. 2003

American Journal of Physiology-Cell Physiology

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. Calcineurinindependent regulation of plasma membrane Ca 2ϩ ATPase-4 in the vascular smooth muscle cell cycle. Am J Physiol Cell Physiol 285: C88-C95, 2003; 10.1152/ajpcell.00518.2002.-Calcineurin mediates repression of plasma membrane Ca 2ϩ -ATPase-4 (PMCA4) expression in neurons, whereas c-Myb is known to repress PMCA1 expression in vascular smooth muscle cells (VSMC). Here, we describe a novel mouse VSMC line (MOVAS) in which 45 Ca efflux rates decreased 50%, fura 2-AM-based intracellular Ca 2ϩ concentrations ([Ca 2ϩ ]i) increased twofold, and real-time RT-PCR and Western blot revealed a ϳ40% decrease in PMCA4 expression levels from G 0 to G1/S in the cell cycle, where PMCA4 constituted ϳ20% of total PMCA protein. Although calcineurin activity increased fivefold as MOVAS progressed from G0 to G1/S, inhibition of this increase with either BAPTA or retroviral transduction with peptide inhibitors of calcineurin (CAIN), or its downstream target nuclear factor of activated T cells (NFAT) (VIVIT), had no effect on the repression of PMCA4 mRNA expression at G1/S. By contrast, Ca 2ϩ -independent activity of the calmodulin-dependent protein kinase-II (CaMK-II) increased eightfold as MOVAS progressed from G0 to G1/S, and treatment with an inhibitor of CaMK-II (KN-93) or transduction of a c-Myb-neutralizing antibody significantly alleviated the G1/S-associated repression of PMCA4. These data show that G1/S-specific PMCA4 repression in proliferating VSMC is brought about by c-Myb and CaMK-II and that calcineurin may regulate cell cycle-associated [Ca 2ϩ ]i through alternate targets. /calmodulin-mediated signals act at multiple points in the cell cycle, including the G 0 /G 1 transition, the initiation of S-phase, and the initiation and completion of M phase (reviewed in Refs. 4,31,38,and 44 ] i ) needed for G 1 -to-S transitions in rat vascular smooth muscle cells (VSMC) (22, 23).We previously showed that the cell cycle-associated repression of PMCA1 expression during G 0 to G 1 /S progression in rat VSMC is mediated by the c-Myb transcription factor (1). However, the mechanism(s) underlying the cell cycle-associated repression of PMCA4 had not been elucidated. Guerini et al. (18) demonstrated in mouse neurons that PMCA4 expression can be repressed by a calcineurin-dependent pathway. Given this result, we hypothesized that G 1 /Sassociated repression of PMCA4 expression in VSMC may also be mediated by calcineurin. To explore these mechanisms in cell culture, we generated a clonal, immortalized mouse VSMC line (MOVAS). Immunostaining for smooth muscle-specific proteins such as SM22␣, calponin, smooth muscle-specific ␣-actin and desmin, as well as SM22␣ promoter-driven enhanced green fluorescent protein (EGFP) expression, confirm the lineage and phenotype of these cells. 45 Ca efflux assays and fura 2-based ratiometric Ca 2ϩ imaging reveal regulated Ca 2ϩ efflux and [Ca 2ϩ ] i at the G 1 /S transition point. Western blot and real time RT-PCR reveal cell cycle-regulated repression of mouse PMCA1 and PMCA4. Drugs in...

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“…PMCA4 is expressed later in development than PMCA1 but is expressed more or less ubiquitously in adult mammalian organs (4). PMCA gene transcription is controlled by c-Myb, leading to changes in the free intracellular Ca 2ϩ concentration ([Ca 2ϩ ] i ) during the cell cycle progression of vascular smooth muscle cells (VSMC) (7)(8)(9).…”

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Calcium Efflux Activity of Plasma Membrane Ca2+ ATPase-4 (PMCA4) Mediates Cell Cycle Progression in Vascular Smooth Muscle Cells

Afroze

Yang

Khoshbin

et al. 2014

Journal of Biological Chemistry

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Background: PMCA4 actions in vascular smooth muscle are not understood. Results: Alternative splicing of PMCA4 changes during vessel injury. Cell cycle arrest and downstream effectors of PMCA4 deletion are rescued by PMCA4a, PMCA4b, and PMCA4b unable to bind PDZ-proteins but not by inactive PMCA4. Conclusion: Ca 2ϩ efflux activity of PMCA4 regulates G 1 progression. Significance: PMCA4 Ca 2ϩ efflux regulates cell cycle.

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c-Myb-binding Sites Mediate G1/S-associated Repression of the Plasma Membrane Ca2+-ATPase-1 Promoter

Cited by 38 publications

References 66 publications

MiR-148a promotes apoptosis by targeting Bcl-2 in colorectal cancer

MiR-148a promotes apoptosis by targeting Bcl-2 in colorectal cancer

Calcineurin-independent regulation of plasma membrane Ca²⁺ ATPase-4 in the vascular smooth muscle cell cycle

Calcium Efflux Activity of Plasma Membrane Ca2+ ATPase-4 (PMCA4) Mediates Cell Cycle Progression in Vascular Smooth Muscle Cells

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c-Myb-binding Sites Mediate G1/S-associated Repression of the Plasma Membrane Ca2+-ATPase-1 Promoter

Cited by 38 publications

References 66 publications

MiR-148a promotes apoptosis by targeting Bcl-2 in colorectal cancer

MiR-148a promotes apoptosis by targeting Bcl-2 in colorectal cancer

Calcineurin-independent regulation of plasma membrane Ca2+ ATPase-4 in the vascular smooth muscle cell cycle

Calcium Efflux Activity of Plasma Membrane Ca2+ ATPase-4 (PMCA4) Mediates Cell Cycle Progression in Vascular Smooth Muscle Cells

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Calcineurin-independent regulation of plasma membrane Ca²⁺ ATPase-4 in the vascular smooth muscle cell cycle