The carboxyterminal processing protease of D1 protein: expression, purification and enzymology of the recombinant and native spinach proteins

2005 ◽  
Vol 61 (7) ◽  
pp. 682-690 ◽  
Author(s):  
Bradon J Fabbri ◽  
Stephen MG Duff ◽  
Edward E Remsen ◽  
Yun-Chia Sophia Chen ◽  
John C Anderson ◽  
...  
Keyword(s):  
Protein Expression ◽  
D1 Protein ◽  
Processing Protease

mTOR function in skeletal muscle hypertrophy: increased ribosomal RNA via cell cycle regulators

2005 ◽  
Vol 289 (6) ◽  
pp. C1457-C1465 ◽  
Author(s):  
Gustavo A. Nader ◽  
Thomas J. McLoughlin ◽  
Karyn A. Esser
Keyword(s):  
Cell Cycle ◽  
Protein Expression ◽  
Cyclin D1 ◽  
Ribosomal Rna ◽  
Molecular Mechanisms ◽  
D1 Protein ◽  
Rna Content ◽  
Cyclin D1 Protein ◽  
Rb Phosphorylation ◽  
Myotube Hypertrophy

The purpose of this study was to identify the potential downstream functions associated with mammalian target of rapamycin (mTOR) signaling during myotube hypertrophy. Terminally differentiated myotubes were serum stimulated for 3, 6, 12, 24, and 48 h. This treatment resulted in significant myotube hypertrophy (protein/DNA) and increased RNA content (RNA/DNA) with no changes in DNA content or indices of cell proliferation. During myotube hypertrophy, the increase in RNA content was accompanied by an increase in tumor suppressor protein retinoblastoma (Rb) phosphorylation and a corresponding increase in the availability of the ribosomal DNA transcription factor upstream binding factor (UBF). Serum stimulation also induced an increase in cyclin D1 protein expression in the differentiated myotubes with a concomitant increase in cyclin D1-dependent cyclin-dependent kinase (CDK)-4 activity toward Rb. The increases in myotube hypertrophy and RNA content were blocked by rapamycin treatment, which also prevented the increase in cyclin D1 protein expression, CDK-4 activity, Rb phosphorylation, and the increase in UBF availability. Our findings demonstrate that activation of mTOR is necessary for myotube hypertrophy and suggest that the role of mTOR is in part to modulate cyclin D1-dependent CDK-4 activity in the regulation of Rb and ribosomal RNA synthesis. On the basis of these results, we propose that common molecular mechanisms contribute to the regulation of myotube hypertrophy and growth during the G1 phase of the cell cycle.

The carboxyterminal processing protease of D1 protein: Herbicidal activity of novel inhibitors of the recombinant and native spinach enzymes

2007 ◽  
Vol 88 (1) ◽  
pp. 1-13 ◽  
Author(s):  
Stephen M.G. Duff ◽  
Yun-Chia Sophia Chen ◽  
Brad J. Fabbri ◽  
Gopichand Yalamanchili ◽  
Bruce C. Hamper ◽  
...  
Keyword(s):  
D1 Protein ◽  
Herbicidal Activity ◽  
Processing Protease

scholarly journals Dehydroepiandrosterone Administration or Gαq Overexpression Induces β-Catenin/T-Cell Factor Signaling and Growth via Increasing Association of Estrogen Receptor-β/Dishevelled2 in Androgen-Independent Prostate Cancer Cells

Endocrinology ◽  
2010 ◽  
Vol 151 (4) ◽  
pp. 1428-1440 ◽  
Author(s):  
Xunxian Liu ◽  
Julia T. Arnold ◽  
Marc R. Blackman
Keyword(s):  
Prostate Cancer ◽  
Estrogen Receptor ◽  
T Cell ◽  
Cell Growth ◽  
Protein Expression ◽  
Cyclin D1 ◽  
D1 Protein ◽  
Nutritional Supplement ◽  
T Cell Factor ◽  
Androgen Independent

β-Catenin/T-cell factor signaling (β-CTS) plays multiple critical roles in carcinogenesis and is blocked by androgens in androgen receptor (AR)-responsive prostate cancer (PrCa) cells, primarily via AR sequestration of β-catenin from T-cell factor. Dehydroepiandrosterone (DHEA), often used as an over-the-counter nutritional supplement, is metabolized to androgens and estrogens in humans. The efficacy and safety of unregulated use of DHEA are unclear. We now report that DHEA induces β-CTS via increasing association of estrogen receptor (ER)-β with Dishevelled2 (Dvl2) in AR nonresponsive human PrCa DU145 cells, a line of androgen-independent PrCa (AiPC) cells. The induction is temporal, as assessed by measuring kinetics of the association of ERβ/Dvl2, protein expression of the β-CTS targeted genes, c-Myc and cyclin D1, and cell growth. However, in PC-3 cells, another human AiPC cell line, DHEA exerts no detectible effects, partly due to their lower expression of Gα-subunits and DHEA down-regulation of ERβ/Dvl2 association. When Gαq is overexpressed in PC-3 cells, β-CTS is constitutively induced, including increasing c-Myc and cyclin D1 protein expression. This effect involved increasing associations of Gαq/Dvl2 and ERβ/Dvl2 and promoted cell growth. These activities require ERβ in DU-145 and PC-3 cells because they are blocked by ICI 182–780 treatment inactivating ERβ, small interfering RNA administration depleting ERβ, or AR overexpression arresting ERβ. These data suggest that novel pathways activating β-CTS play roles in the progression of AiPC. Although DHEA may enhance PrCa cell growth via androgenic or estrogenic pathways, the effects of DHEA administration on clinical prostate function remain to be determined.

Cyclin D1 protein expression and function in human breast cancer

1994 ◽  
Vol 57 (3) ◽  
pp. 353-361 ◽  
Author(s):  
Jirina Bartkova ◽  
Jiri Lukas ◽  
Heiko Müller ◽  
Dorrit Lützhøt ◽  
Michael Strauss ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Protein Expression ◽  
Cyclin D1 ◽  
Human Breast Cancer ◽  
D1 Protein ◽  
Human Breast ◽  
Cyclin D1 Protein ◽  
And Function

scholarly journals Requirement of Cyclin D1 in Mesangial Cell Mitogenesis

2000 ◽  
Vol 11 (8) ◽  
pp. 1398-1408
Author(s):  
STEFAN LANG ◽  
ANDREA HARTNER ◽  
R. BERND STERZEL ◽  
HARALD O. SCHÖCKLMANN
Keyword(s):  
Growth Factor ◽  
Protein Expression ◽  
Cyclin D1 ◽  
Transforming Growth Factor ◽  
D1 Protein ◽  
Transforming Growth Factor Β1 ◽  
Protein Levels ◽  
Cyclin D1 Protein

Abstract. Hyperplasia of mesangial cells (MC) is a frequent finding in glomerulonephritis. The control and function of cyclin D1, a regulator of cell cycle progression, in MC proliferation in vivo and in vitro were investigated. In a rat model of mesangioproliferative glomerulonephritis, increases in the number of cyclin D1-positive MC nuclei were prominent on day 5 of the disease, preceding the peak of MC hyperplasia. In growth-arrested rat MC in culture, mitogenic stimulation with serum or platelet-derived growth factor (PDGF) led to rapid increases in cyclin D1 protein expression. Transforming growth factor-β1 inhibited PDGF induction of cyclin D1 protein at 12 h. In an examination of the subcellular distribution of cyclin D1, it was observed that stimulation of MC with PDGF for 6 h caused translocation of cyclin D1 from the cytoplasm into the nucleus. Coincubation with PDGF and transforming growth factor-β1 completely inhibited this effect, without altering the cellular cyclin D1 protein abundance at that time point. To test whether reduction of cyclin D1 protein levels was sufficient to inhibit mitogenesis, MC were transfected with antisense oligonucleotides (ODN) complementary to rat cyclin D1 mRNA. Antisense ODN against cyclin D1 reduced the serum- or PDGF-induced protein expression of cyclin D1 to 27 or 10% of control levels, respectively. These inhibitory effects were correlated with diminished cyclin-dependent kinase 4 activity. Antisense ODN against cyclin D1 also decreased the PDGF-induced increase in p21Waf-1 protein levels. The MC proliferation caused by serum or PDGF was markedly inhibited by antisense ODN against cyclin D1, as measured by [3H]thymidine uptake and cell counts. It is concluded that increased cyclin D1 protein expression of MC is required for MC proliferation. Targeting cyclin D1 expression may represent an effective means to inhibit MC proliferation in vitro and in vivo.

scholarly journals Splenic B-Cell Lymphomas with Diffuse Cyclin D1 Protein Expression and Increased Prolymphocytic Cells: A Previously Unrecognized Diagnostic Pitfall

2018 ◽  
Vol 2018 ◽  
pp. 1-9
Author(s):  
Khaled Algashaamy ◽  
Yaohong Tan ◽  
Nicolas Mackrides ◽  
Alvaro Alencar ◽  
Jing-Hong Peng ◽  
...  
Keyword(s):  
Protein Expression ◽  
B Cell ◽  
Cyclin D1 ◽  
D1 Protein ◽  
Diagnostic Errors ◽  
Lymphocytic Leukemia ◽  
Splenic Marginal Zone Lymphoma ◽  
B Cell Lymphomas ◽  
Prolymphocytic Leukemia ◽  
Diagnostic Pitfall

Prolymphocytic transformation is a concept usually applied in the context of chronic lymphocytic leukemia/small lymphocytic lymphoma to describe the presence of a high percentage of prolymphocytes in peripheral blood (usually more than 55%). Prolymphocytic transformation has also been reported in mantle cell lymphoma (MCL) but only rarely in splenic marginal zone lymphoma (SMZL). We present two splenic B-cell lymphomas presenting in the leukemic phase and with increased prolymphocytes, both classified as SMZL with prolymphocytic transformation. One case clinically simulated B-prolymphocytic leukemia (B-PLL). Both lymphomas were very unusual because the tumor cells diffusely and strongly expressed cyclin D1 despite lacking the t(11; 14)(q13; q32) as detected by several approaches including next-generation sequencing, fluorescence in situ hybridization using CCND1 break apart probe and fusion probes for t(11; 14)(q13; q32), and conventional karyotyping. These cases therefore simulated prolymphocytic variants of MCL. The incidence of this phenomenon is unknown, and awareness of this potential alternate protein expression pattern is important in order to avoid diagnostic errors.

scholarly journals Cyclin D1 differential activation and its prognostic impact in patients with advanced breast cancer treated with trastuzumab

ESMO Open ◽  
2019 ◽  
Vol 4 (2) ◽  
pp. e000441 ◽  
Author(s):  
G Mountzios ◽  
Vassiliki Kotoula ◽  
Georgia-Angeliki Kolliou ◽  
Kyriaki Papadopoulou ◽  
Georgios Lazaridis ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Protein Expression ◽  
Advanced Breast Cancer ◽  
Cyclin D1 ◽  
Prognostic Significance ◽  
D1 Protein ◽  
Advanced Breast ◽  
Prognostic Impact ◽  
Her2 Positive ◽  
Risk Of Progression

IntroductionWe sought to determine the level of activation of the critical components of the cyclin D1-mediated pathway and to evaluate their prognostic significance across the different molecular subtypes of advanced breast cancer.Patients and methodsThe study population comprised 219 female patients with advanced breast cancer who had been found to have human epidermal growth factor receptor 2 (HER2)-positive disease by local testing and were all treated with trastuzumab-based regimens. For all tumours, central testing for HER2 was performed, and cyclin D1 gene (CCND1) amplification, mRNA and protein expression were assessed by FISH, quantitative real-time-PCR and immunohistochemistry, respectively. Prognostic impact on clinical endpoints was evaluated with Cox regression analyses.ResultsAfter central testing, only 134 (61.2%) of 219 patients were confirmed to have HER2 gene amplification by FISH and/or 3+ HER2 protein expression by immunohistochemistry. After a median follow-up time of 136.0 months (95% CI 123.3 to 148.9), 105 (78.4%) HER2-positive patients and 76 (89.4%) HER2-negative patients had died, while 80% of the former and 87.1% of the latter had experienced a disease relapse. Patients with positive oestrogen receptor/progesterone receptor status presented with higher cyclin D1 mRNA expression. In the HER2-negative subgroup, patients with negative cyclin D1 protein expression were at higher risk of progression (HR= 1.66, 95%CI 1.01 to 2.72, Wald’s p=0.045). Among de novo metastatic patients, the risk of progression was higher for patients with non-amplified CCND1 tumours (HR= 2.00, 95% CI 1.03 to 3.90, p=0.041).ConclusionAberrant activation of the cyclin D1-mediated pathway appears to reduce the risk of progression in HER2-negative tumours, but not in HER2-positive ones.

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