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Artykuły w czasopismach na temat „D1 cells”

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Data publikacji: 3 czerwca 2025

Data aktualizacji: 31 lipca 2025

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1

Feng, Hanping, Yi Zeng, Michael W. Graner, and Emmanuel Katsanis. "Stressed apoptotic tumor cells stimulate dendritic cells and induce specific cytotoxic T cells." Blood 100, no. 12 (2002): 4108–15. http://dx.doi.org/10.1182/blood-2002-05-1389.

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We have previously reported that stressed apoptotic tumor cells are more immunogenic in vivo than nonstressed ones. Using confocal microscopy we have confirmed our previous observation that heat-stressed apoptotic 12B1-D1 leukemia cells(BCR-ABL+) express HSP60 and HSP72 on their surface. To explore how the immune system distinguishes stressed from nonstressed apoptotic tumor cells, we analyzed the responses of dendritic cells to these 2 types of apoptotic cells. We found that nonstressed and heat-stressed apoptotic 12B1-D1 cells were taken up by dendritic cells in a comparable fashion. However

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2

Muraoka, Rebecca S., Anne E. G. Lenferink, Brian Law, et al. "ErbB2/Neu-Induced, Cyclin D1-Dependent Transformation Is Accelerated in p27-Haploinsufficient Mammary Epithelial Cells but Impaired in p27-Null Cells." Molecular and Cellular Biology 22, no. 7 (2002): 2204–19. http://dx.doi.org/10.1128/mcb.22.7.2204-2219.2002.

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ABSTRACT ErbB2/Neu destabilizes the cyclin-dependent kinase (Cdk) inhibitor p27 and increases expression of cyclin D1. Therefore, we studied the roles of p27 and cyclin D1 in ErbB2-mediated mammary epithelial cell transformation. Overexpression of ErbB2 or cyclin D1 in p27+/− primary murine mammary epithelial cells resulted in increased proliferation, cyclin D1 nuclear localization, and colony formation in soft agar compared to those in p27+/+ cells. In contrast, ErbB2- or cyclin D1-overexpressing p27−/− cells displayed reduced proliferation, anchorage-independent growth, Cdk4 activity, cyclin

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3

Zhu, Bo, Ashutosh Shrivastava, Cristina Luongo, et al. "Catalysis leads to posttranslational inactivation of the type 1 deiodinase and alters its conformation." Journal of Endocrinology 214, no. 1 (2012): 87–94. http://dx.doi.org/10.1530/joe-11-0459.

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Previously, it was shown that the type 1 deiodinase (D1) is subject to substrate-dependent inactivation that is blocked by pretreatment with the inhibitor of D1 catalysis, propylthiouracil (PTU). Using HepG2 cells with endogenous D1 activity, we found that while considerable D1-mediated catalysis of reverse tri-iodothyronine (rT3) is observed in intact cells, there was a significant loss of D1 activity in sonicates assayed from the same cells in parallel. This rT3-mediated loss of D1 activity occurs despite no change in D1 mRNA levels and is blocked by PTU treatment, suggesting a requirement f

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4

Rosenwald, I. B., A. Lazaris-Karatzas, N. Sonenberg, and E. V. Schmidt. "Elevated levels of cyclin D1 protein in response to increased expression of eukaryotic initiation factor 4E." Molecular and Cellular Biology 13, no. 12 (1993): 7358–63. http://dx.doi.org/10.1128/mcb.13.12.7358-7363.1993.

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Cyclin D1 is a G1-specific cyclin that has been linked to lymphoid, parathyroid, and breast tumors. Recent studies suggested that high protein levels of cyclin D1 are not always produced when cyclin D1 mRNA is overexpressed in transfected cells, suggesting that posttranscriptional events may be important in cyclin D1 regulation. The mRNA cap-binding protein (eukaryotic initiation factor 4E [eIF-4E]) is a potential regulatory of several posttranscriptional events, and it can itself induce neoplastic transformation. Consequently, we examined eIF-4E as a potential regulator of cyclin D1. Overexpr

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5

Rosenwald, I. B., A. Lazaris-Karatzas, N. Sonenberg, and E. V. Schmidt. "Elevated levels of cyclin D1 protein in response to increased expression of eukaryotic initiation factor 4E." Molecular and Cellular Biology 13, no. 12 (1993): 7358–63. http://dx.doi.org/10.1128/mcb.13.12.7358.

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Cyclin D1 is a G1-specific cyclin that has been linked to lymphoid, parathyroid, and breast tumors. Recent studies suggested that high protein levels of cyclin D1 are not always produced when cyclin D1 mRNA is overexpressed in transfected cells, suggesting that posttranscriptional events may be important in cyclin D1 regulation. The mRNA cap-binding protein (eukaryotic initiation factor 4E [eIF-4E]) is a potential regulatory of several posttranscriptional events, and it can itself induce neoplastic transformation. Consequently, we examined eIF-4E as a potential regulator of cyclin D1. Overexpr

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6

Ladha, Mohamed H., Kwang Y. Lee, Todd M. Upton, Michael F. Reed, and Mark E. Ewen. "Regulation of Exit from Quiescence by p27 and Cyclin D1-CDK4." Molecular and Cellular Biology 18, no. 11 (1998): 6605–15. http://dx.doi.org/10.1128/mcb.18.11.6605.

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ABSTRACT The synthesis of cyclin D1 and its assembly with cyclin-dependent kinase 4 (CDK4) to form an active complex is a rate-limiting step in progression through the G1 phase of the cell cycle. Using an activated allele of mitogen-activated protein kinase kinase 1 (MEK1), we show that this kinase plays a significant role in positively regulating the expression of cyclin D1. This was found both in quiescent serum-starved cells and in cells expressing dominant-negative Ras. Despite the observation that cyclin D1 is a target of MEK1, in cycling cells, activated MEK1, but not cyclin D1, is capab

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7

Epner, Elliot M., Hui Liu, Jing Wang, and Mathew Thayer. "Transvection Mediated by the Translocated Cyclin D1 Gene in Mantle Cell Lymphoma." Blood 110, no. 11 (2007): 4156. http://dx.doi.org/10.1182/blood.v110.11.4156.4156.

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Abstract Cyclin D1 expression in B cells is deregulated by chromosome translocations involving the immunoglobulin heavy chain (IgH) locus in mantle cell lymphoma (MCL). Gene targeting experiments produced MCL cell lines that had lost the translocated t(11;14) and no longer expressed cyclin D1. In these cyclin D1 (−) cells, the nonrearranged cyclin D1 (CCND1) locus reverts from CpG hypomethylated to hypermethylated. Reintroduction of the translocated chromosome by somatic cell hybrid fusion induces loss of methylation at the unrearranged CCND1 locus. Thus, the translocated chromosome exerts a t

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8

Zwijsen, R. M., R. Klompmaker, E. B. Wientjens, P. M. Kristel, B. van der Burg, and R. J. Michalides. "Cyclin D1 triggers autonomous growth of breast cancer cells by governing cell cycle exit." Molecular and Cellular Biology 16, no. 6 (1996): 2554–60. http://dx.doi.org/10.1128/mcb.16.6.2554.

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Cyclin D1 controls G1-associated processes, including G0-to-G1 and G1-to-S transitions. This study demonstrates a novel aspect of cyclin D1 as a regulator of the transition between G1 and G0. Overexpression of cyclin D1 in MCF7 breast tumor cells resulted in a continued proliferation under low-serum conditions, whereas nonoverexpressing cells ceased to grow. This difference in growth was due to a reduced exit from G1 to G0 in cyclin D1-overexpressing cells. Our data therefore suggest a model in which cyclin D1 overexpression in tumor cells is responsible for hyperproliferation under growth fac

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9

Flood, Michael D., Johnnie M. Moore-Dotson, and Erika D. Eggers. "Dopamine D1 receptor activation contributes to light-adapted changes in retinal inhibition to rod bipolar cells." Journal of Neurophysiology 120, no. 2 (2018): 867–79. http://dx.doi.org/10.1152/jn.00855.2017.

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Dopamine modulation of retinal signaling has been shown to be an important part of retinal adaptation to increased background light levels, but the role of dopamine modulation of retinal inhibition is not clear. We previously showed that light adaptation causes a large reduction in inhibition to rod bipolar cells, potentially to match the decrease in excitation after rod saturation. In this study, we determined how dopamine D1 receptors in the inner retina contribute to this modulation. We found that D1 receptor activation significantly decreased the magnitude of inhibitory light responses fro

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10

Mori, Kazunori, Etsuko Hirao, Yosuke Toya, et al. "Competitive Nuclear Export of Cyclin D1 and Hic-5 Regulates Anchorage Dependence of Cell Growth and Survival." Molecular Biology of the Cell 20, no. 1 (2009): 218–32. http://dx.doi.org/10.1091/mbc.e08-04-0428.

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Anchorage dependence of cell growth and survival is a critical trait that distinguishes nontransformed cells from transformed cells. We demonstrate that anchorage dependence is determined by anchorage-dependent nuclear retention of cyclin D1, which is regulated by the focal adhesion protein, Hic-5, whose CRM1-dependent nuclear export counteracts that of cyclin D1. An adaptor protein, PINCH, interacts with cyclin D1 and Hic-5 and potentially serves as an interface for the competition between cyclin D1 and Hic-5 for CRM1. In nonadherent cells, the nuclear export of Hic-5, which is redox-sensitiv

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11

Wilhide, CC, C. Van Dang, J. Dipersio, AA Kenedy, and PF Bray. "Overexpression of cyclin D1 in the Dami megakaryocytic cell line causes growth arrest." Blood 86, no. 1 (1995): 294–304. http://dx.doi.org/10.1182/blood.v86.1.294.bloodjournal861294.

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The maturation of megakaryocytes in vivo requires polyploidization or repeated duplication of DNA without cytokinesis. As DNA replication and cytokinesis are tightly regulated in somatic cells by cyclins and cyclin-dependent kinases, we sought to determine the pattern of cyclin gene expression in cells that undergo megakaryocytic differentiation and polyploidization. The Dami megakaryocytic cell line differentiates and increases ploidy in response to phorbol 12-myristate 13-acetate (PMA) stimulation in vitro. We used Northern blotting to analyze mRNA levels of cyclins A, B, C, D1, and E in PMA

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12

Kuroda, Yoshiaki, Akira Sakai, Naohiro Tsuyama, et al. "Cyclin D1 Overexpression Increases Chemosensitivity Via the Induction of Bim in Myeloma Cells." Blood 108, no. 11 (2006): 3418. http://dx.doi.org/10.1182/blood.v108.11.3418.3418.

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Abstract Recent study analyzing the gene expression in myeloma cells using cDNA microarray showed that myeloma cells are divided into 7 groups. Two showed a high expression of cyclin D1 together with a low expression of cyclin D2, and they belong to the low-risk group when analyzed based on event-free and overall survival. Since cyclin D1 promotes the cell cycle progression, we sought to explain why cyclin D1 overexpression appears to be a favorable prognostic variable for multiple myeloma (MM) patients treated with high-dose chemotherapy and single or double autologous transplantation. It is

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13

Kahl, Christina R., and Anthony R. Means. "Calcineurin Regulates Cyclin D1 Accumulation in Growth-stimulated Fibroblasts." Molecular Biology of the Cell 15, no. 4 (2004): 1833–42. http://dx.doi.org/10.1091/mbc.e03-10-0730.

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Calcium (Ca2+) and calmodulin (CaM) are required for progression of mammalian cells from quiescence into S phase. In multiple cell types, cyclosporin A causes a G1 cell cycle arrest, implicating the serine/threonine phosphatase calcineurin as one Ca2+/CaM-dependent enzyme required for G1 transit. Here, we show, in diploid human fibroblasts, that cyclosporin A arrested cells in G1 before cyclin D/cdk4 complex activation and retinoblastoma hyperphosphorylation. This arrest occurred in early G1 with low levels of cyclin D1 protein. Because cyclin D1 mRNA was induced normally in the cyclosporin A-

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14

Kuroda, Yoshiaki, Akira Sakai, Naohiro Tsuyama, et al. "Cyclin D1 Overexpression Increases Chemosensitivity Via Prolonged S-Phase and TRAIL Signal in Myeloma Cell." Blood 110, no. 11 (2007): 3530. http://dx.doi.org/10.1182/blood.v110.11.3530.3530.

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Abstract The mechanism of oncogenesis of plasma cells remains unclear. Since tumor cells are post-germinal center B cells, reciprocal chromosomal translocations between the IgH gene located on chromosome 14q32 and other chromosomal partners such as cyclin D1 located on chromosome 11q23, which are supposed to be candidate oncogene, arise in myeloma cells during the procedure of isotype switching. However, a recent study demonstrated that multiple myeloma (MM) with cyclin D1 overexpression belongs to the low-risk group. Previously, we reported that cyclin D1 overexpression downregulated cyclin D

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15

Stuart, August, Sara Shimko, and Elliot M. Epner. "Crosstalk Between Cyclins D1 and D3 in Mantle Cell Level At the Transcriptional and Postranscriptional Levels." Blood 118, no. 21 (2011): 1373. http://dx.doi.org/10.1182/blood.v118.21.1373.1373.

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Abstract Abstract 1373 Cyclin D1 (CCND1) expression is deregulated epigenetically in mantle cell lymphoma by the t(11;14) chromosome translocation. We have investigated the phenomenon of cyclin D1 mediated oncogene addiction in mantle cell lymphoma (MCL) and multiple myeloma (MM) cell lines. Gene targeting methods were utilized to generate Cyclin D1(-) MCL and MM cell lines. These cell lines did not make any detectable cyclin D1 mRNA and protein. These cells lines had shorter doubling times in vitro than their cyclin D1(+) counterparts and were also more chemoresistant in vitro and more tumori

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Kuroda, Yoshiaki, Akira Sakai, Naohiro Tsuyama, et al. "Induction of Cyclin D1 Gene in Myeloma Cells Down-Regulates the Expression of Cyclin D2." Blood 106, no. 11 (2005): 3411. http://dx.doi.org/10.1182/blood.v106.11.3411.3411.

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Abstract Cyclin D is dysregulated in at least two-thirds of multiple myeloma (MM) tumors. In addition, recent reports showed that the dysregulation of cyclin D1 is frequent in the absence of a t(11;14) translocation in MM. However, as we also reported (Int J Oncol, 2004), there appears to be no obvious correlation between the expression of cyclin D1 and the proliferation index (PI) or Ki67 expression. Therefore, we thought that the down-regulation of cyclin D2 might offset the expression of cyclin D1 in myeloma cells with cyclin D1 overexpression in cDNA microarray, since primary myeloma cells

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17

Lukas, J., H. Müller, J. Bartkova, et al. "DNA tumor virus oncoproteins and retinoblastoma gene mutations share the ability to relieve the cell's requirement for cyclin D1 function in G1." Journal of Cell Biology 125, no. 3 (1994): 625–38. http://dx.doi.org/10.1083/jcb.125.3.625.

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The retinoblastoma gene product (pRB) participates in the regulation of the cell division cycle through complex formation with numerous cellular regulatory proteins including the potentially oncogenic cyclin D1. Extending the current view of the emerging functional interplay between pRB and D-type cyclins, we now report that cyclin D1 expression is positively regulated by pRB. Cyclin D1 mRNA and protein is specifically downregulated in cells expressing SV40 large T antigen, adenovirus E1A, and papillomavirus E7/E6 oncogene products and this effect requires intact RB-binding, CR2 domain of E1A.

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Wang, Michael, Luhong Sun, Jianfei Qian, et al. "Cyclin D1 as a Universally-Expressed Mantle Cell Lymphoma-Associated aTumor Antigen for Immunotherapy." Blood 112, no. 11 (2008): 882. http://dx.doi.org/10.1182/blood.v112.11.882.882.

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Abstract Mantle cell lymphoma (MCL) accounts for 5% to 10% of all non-Hodgkin lymphomas and has the worst prognosis among all lymphomas. The hallmark of MCL is a t(11;14) translocation resulting in overexpression of cyclin D1 by tumor cells of virtually all patients. In this study we examined whether cyclin D1 could be an effective tumor-associated antigen for immunotherapy. We identified a cyclin D1 peptide (P101) for HLA-A*0201, created heteroclitic peptide (Py101) for better binding, and generated peptide-specific T-cell lines from HLA-A*0201+ blood donors and MCL patients. After 5 to 7 rou

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Lee, Richard J., Chris Albanese, Maofu Fu, et al. "Cyclin D1 Is Required for Transformation by Activated Neu and Is Induced through an E2F-Dependent Signaling Pathway." Molecular and Cellular Biology 20, no. 2 (2000): 672–83. http://dx.doi.org/10.1128/mcb.20.2.672-683.2000.

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ABSTRACT The neu (c-erbB-2) proto-oncogene encodes a tyrosine kinase receptor that is overexpressed in 20 to 30% of human breast tumors. Herein, cyclin D1 protein levels were increased in mammary tumors induced by overexpression of wild-type Neu or activating mutants of Neu in transgenic mice and in MCF7 cells overexpressing transforming Neu. Analyses of 12 Neu mutants in MCF7 cells indicated important roles for specific C-terminal autophosphorylation sites and the extracellular domain in cyclin D1 promoter activation. Induction of cyclin D1 by NeuT involved Ras, Rac, Rho, extracellular signal

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Liu, J. J., J. R. Chao, M. C. Jiang, S. Y. Ng, J. J. Yen, and H. F. Yang-Yen. "Ras transformation results in an elevated level of cyclin D1 and acceleration of G1 progression in NIH 3T3 cells." Molecular and Cellular Biology 15, no. 7 (1995): 3654–63. http://dx.doi.org/10.1128/mcb.15.7.3654.

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Ectopic overexpression of v-H-Ras protein in NIH 3T3 cells resulted in cellular transformation and an acceleration of G1 progression of these cells. A shortened G1 phase was found to be associated with an increased level of cyclin D1 but not cyclin E protein. Using an antisense blocking method, reduced synthesis of cyclin D1 in v-H-Ras transformants resulted in a slower G1 progression rate of these cells. Although constitutive overexpression of cyclin D1 in NIH 3T3 cells accelerated G1 progression, cells remained untransformed. Furthermore, inhibition of cyclin D1 synthesis greatly impaired th

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Smith, Dean, Kwee L. Yong, and David Mann. "Cell Cycle Responses of Cyclin D1 and D2-Bearing Multiple Myeloma Tumours to DNA Damage Caused By Ionising Radiation." Blood 124, no. 21 (2014): 2011. http://dx.doi.org/10.1182/blood.v124.21.2011.2011.

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Abstract Introduction: Multiple Myeloma (MM) tumours are characterised by dysregulated expression of a D-type cyclin, usually either D1 or D2. Tumours expressing D1 or D2 fall into distinct genetic subtypes, distinguished by transcriptome profiles and clinical features, including outcomes of therapy. D-type cyclins control entry to the cell cycle, and we have previously shown that cell cycle entry is regulated differently in D1 versus D2 tumours (Glassford et al, 2007, 2012, Quinn et al, 2011), but little is known of how these tumours differ in the cell cycle response to DNA damaging agents, u

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Jiao, Xuanmao, Chongwen Xu, Lifeng Tian, et al. "Abstract P3-10-03: Enrichment of pro-oncogenic immune miRNAs in exosomes by cyclin D1, promote cancer stem cell expansion." Cancer Research 82, no. 4_Supplement (2022): P3–10–03—P3–10–03. http://dx.doi.org/10.1158/1538-7445.sabcs21-p3-10-03.

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Abstract The cyclin D1 (CCND1) gene, encodes the regulatory subunit of a holoenzyme that phosphorylates and inactivates the Rb protein. Cyclin D1 overexpression occurs in up to 50% of human breast cancers. Cyclin D1, governs the expression (1,3), processing (2), the secretion and the relative proportion of secreted non-coding RNA subtypes (miRNA, rRNA, tRNA, CDBox, scRNA, HAcaBox. scaRNA, piRNA) in human breast cancer and the secretion of piRNA (4). Through base-pairing to the complementary sequence in 3’ untranslated region (3’ UTR) of mRNA, miRNAs participate in diverse biological processes.

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Bolner, Michelle, Pamela Fink, and Ellen Richie. "Preventing thymus involution in K5.Cyclin D1 transgenic mice sustains the naïve T cell compartment with age (LYM6P.716)." Journal of Immunology 194, no. 1_Supplement (2015): 135.4. http://dx.doi.org/10.4049/jimmunol.194.supp.135.4.

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Abstract The thymus maintains T cell receptor (TCR) repertoire diversity through perpetual release of self-MHC restricted naive T cells. However, thymus involution during the aging process reduces naïve T cell output, leading to defective immune responsiveness to newly encountered antigens. We have shown that age-related thymus involution is prevented in mice expressing a keratin 5 promoter-driven Cyclin D1 (K5.D1) transgene in thymic epithelial cells (TECs). Sustained T cell output from K5.D1 thymi prevents the age-associated decline of naïve T cells in the periphery. We find that K5.D1 recen

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Häussler, Ulla, Götz von Wichert, Roland M. Schmid, Frieder Keller та Günter Schneider. "Epidermal growth factor activates nuclear factor-κB in human proximal tubule cells". American Journal of Physiology-Renal Physiology 289, № 4 (2005): F808—F815. http://dx.doi.org/10.1152/ajprenal.00434.2003.

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The promotion of cell survival and regeneration in acute renal failure (ARF) is important for the restitution of renal function. Epidermal growth factor (EGF) has been implicated in the regulation of cell proliferation. We provide evidence for a direct link between EGF, nuclear factor-κB (NF-κB), and cell cycle regulation (cyclin D1). EGF was found to stimulate NF-κB-dependent gene transcription and DNA binding. In addition, EGF stimulated cyclin D1 promoter activity as well as cyclin D1 expression. Moreover, inhibition of NF-κB caused a pronounced reduction of EGF-induced cyclin D1 promoter a

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Ewanowich, Carol, Russell K. Brynes, L. Jeffrey Medeiros, Althea McCourty, and Raymond Lai. "Cyclin D1 Expression in Dysplastic Nevi." Archives of Pathology & Laboratory Medicine 125, no. 2 (2001): 208–10. http://dx.doi.org/10.5858/2001-125-0208-cdeidn.

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Abstract Objective.—We previously surveyed cyclin D1 expression in common acquired nevi, Spitz nevi, and malignant melanomas and reported that benign nevi maintain a zonal pattern of cyclin D1 expression, in contrast with malignant melanomas. Our aim was to extend those observations by examining cyclin D1 expression in dysplastic nevi. Methods.—Cyclin D1 overexpression in 23 dysplastic nevi was detected by an immunohistochemical technique. The extent of atypia of the nevi was graded as mild, moderate, or severe, using previously established criteria. Results.—Cyclin D1 overexpression in dyspla

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Tian, Min, Ting Lan, Min Gao, Bo Li, Gai Zhang та Hai-Bo Wang. "Synthesis and Characterization of Two Chiral Pyrrolyl α-Nitronyl Nitroxide Radicals and Determination of their Cytotoxicity and Radioprotective Properties in C6 Cells and Mice under Ionizing Radiation". Australian Journal of Chemistry 72, № 7 (2019): 492. http://dx.doi.org/10.1071/ch18625.

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In this study, two chiral nitronyl nitroxyl radicals, L1 and D1, were synthesized and evaluated for their potential radioprotective properties invitro and invivo. We synthesized the new stable nitronyl nitroxide radicals, L1 and D1, according to Ullman’s method, and their chemical structures were characterized using UV-vis absorption, electron spin resonance (ESR), and circular dichroism (CD) spectra. The cytotoxicity of L1 and D1 on C6 glioma cells (C6 cells) was examined using the MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay. To study the anti-radiation effects of

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Szeky, Balázs, B. Mayer, M. Gyongy, et al. "Tri-Lineage Differentiation of NTERA2 Clone D1 Cells towards Neural, Hepatic and Osteogenic Lineages in Vitro." Folia Biologica 67, no. 5-6 (2021): 174–82. http://dx.doi.org/10.14712/fb2021067050174.

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Over the past decades, the in vitro use of pluripotent cell lines gained a crucial role in toxicology, preclinical drug testing and developmental biology. NTERA2 clone D1 cells were identified as pluripotent cells with high potential for neural differentiation. Although they are commonly used cellular sources in neuropharmacology and neurodevelopmental studies, their endodermal and mesodermal differentiation potential awaits further characterization. Here, we devised improved protocols for hepatogenic and osteogenic differentiation of NTERA2 clone D1 cells. Our in vitro differentiation assays

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Mejlvang, Jakob, Marina Kriajevska, Cindy Vandewalle, et al. "Direct Repression of Cyclin D1 by SIP1 Attenuates Cell Cycle Progression in Cells Undergoing an Epithelial Mesenchymal Transition." Molecular Biology of the Cell 18, no. 11 (2007): 4615–24. http://dx.doi.org/10.1091/mbc.e07-05-0406.

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Zinc finger transcription factors of the Snail/Slug and ZEB-1/SIP1 families control epithelial-mesenchymal transitions in development in cancer. Here, we studied SIP1-regulated mesenchymal conversion of epidermoid A431 cells. We found that concomitant with inducing invasive phenotype, SIP1 inhibited expression of cyclin D1 and induced hypophosphorylation of the Rb tumor suppressor protein. Repression of cyclin D1 was caused by direct binding of SIP1 to three sequence elements in the cyclin D1 gene promoter. By expressing exogenous cyclin D1 in A431/SIP1 cells and using RNA interference, we dem

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Xiong, W., R. G. Pestell, G. Watanabe, J. Li, M. R. Rosner, and M. B. Hershenson. "Cyclin D1 is required for S phase traversal in bovine tracheal myocytes." American Journal of Physiology-Lung Cellular and Molecular Physiology 272, no. 6 (1997): L1205—L1210. http://dx.doi.org/10.1152/ajplung.1997.272.6.l1205.

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We examined the role of cyclin D1 in cultured bovine tracheal myocyte mitogenesis. Immunoblots using a polyclonal antibody against cyclin D1 showed the appearance of this protein 4 h after treatment with platelet-derived growth factor (PDGF), a potent mitogen for these cells. Immunoblots utilizing an antibody against the 110-kDa retinoblastoma protein (Rb), a downstream phosphorylation target of the cyclin D1/cyclin-dependent kinase 4 (cdk4) complex, showed reduced electrophoretic mobility of this protein as early as 8 h after PDGF treatment, suggesting phosphorylation of Rb by the cyclin D1/c

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Li, Shixiong, Edward R. Gerrard, and Daniel F. Balkovetz. "Evidence for ERK1/2 phosphorylation controlling contact inhibition of proliferation in Madin-Darby canine kidney epithelial cells." American Journal of Physiology-Cell Physiology 287, no. 2 (2004): C432—C439. http://dx.doi.org/10.1152/ajpcell.00020.2004.

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Increasing cell density arrests epithelial cell proliferation by a process termed contact inhibition. We investigated mechanisms of contact inhibition using a model of contact-inhibited epithelial cells. Hepatocyte growth factor (HGF) treatment of contact-inhibited Madin-Darby canine kidney (MDCK) cells stimulated cell proliferation and increased levels of phosphorylated ERK1/2 (phospho-ERK1/2) and cyclin D1. MEK inhibitors PD-98059 and U0126 inhibited these HGF-dependent changes, indicating the dependence on phosphorylation of ERK1/2 during HGF-induced loss of contact inhibition. In relation

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Wang, Shaoxiong, Xi Lu, Jian Yang, et al. "Regulation of renalase expression by D5 dopamine receptors in rat renal proximal tubule cells." American Journal of Physiology-Renal Physiology 306, no. 6 (2014): F588—F596. http://dx.doi.org/10.1152/ajprenal.00196.2013.

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The dopaminergic and sympathetic systems interact to regulate blood pressure. Our previous studies showed regulation of α1-adrenergic receptor function by D1-like dopamine receptors in vascular smooth muscle cells. Because renalase could regulate circulating epinephrine levels and dopamine production in renal proximal tubules (RPTs), we tested the hypothesis that D1-like receptors regulate renalase expression in kidney. The effect of D1-like receptor stimulation on renalase expression and function was measured in immortalized RPT cells from Wistar-Kyoto (WKY) and spontaneously hypertensive rat

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Hitomi, Masahiro, Ke Yang, Andrew W. Stacey, and Dennis W. Stacey. "Phosphorylation of Cyclin D1 Regulated by ATM or ATR Controls Cell Cycle Progression." Molecular and Cellular Biology 28, no. 17 (2008): 5478–93. http://dx.doi.org/10.1128/mcb.02047-07.

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ABSTRACT Cyclin D1 is required at high levels for passage through G1 phase but must be reduced to low levels during S phase to avoid the inhibition of DNA synthesis. This suppression requires the phosphorylation of Thr286, which is induced directly by DNA synthesis. Because the checkpoint kinase ATR is activated by normal replication as well as by DNA damage, its potential role in regulating cyclin D1 phosphorylation was tested. We found that ATR, activated by either UV irradiation or the topoisomerase IIβ binding protein 1 activator, promoted cyclin D1 phosphorylation. Small interfering RNA a

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Nurtjahja-Tjendraputra, Effie, Dong Fu, Juanita M. Phang, and Des R. Richardson. "Iron chelation regulates cyclin D1 expression via the proteasome: a link to iron deficiency–mediated growth suppression." Blood 109, no. 9 (2006): 4045–54. http://dx.doi.org/10.1182/blood-2006-10-047753.

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Abstract Iron (Fe) plays an important role in proliferation, and Fe deficiency results in G1/S arrest. Despite this, the precise role of Fe in cell-cycle control remains unclear. Cyclin D1 plays a critical function in G1 progression by interacting with cyclin-dependent kinases. Previously, we examined the effect of Fe depletion on the expression of cell-cycle control molecules and identified a marked decrease in cyclin D1 protein, although the mechanism involved was unknown. In this study, we showed that cyclin D1 was regulated posttranscriptionally by Fe depletion. Iron chelation of cells in

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Resnitzky, D. "Ectopic expression of cyclin D1 but not cyclin E induces anchorage-independent cell cycle progression." Molecular and Cellular Biology 17, no. 9 (1997): 5640–47. http://dx.doi.org/10.1128/mcb.17.9.5640.

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Normal fibroblasts are dependent on adhesion to a substrate for cell cycle progression. Adhesion-deprived Rat1 cells arrest in the G1 phase of the cell cycle, with low cyclin E-dependent kinase activity, low levels of cyclin D1 protein, and high levels of the cyclin-dependent kinase inhibitor p27kip1. To understand the signal transduction pathway underlying adhesion-dependent growth, it is important to know whether prevention of any one of these down-regulation events under conditions of adhesion deprivation is sufficient to prevent the G1 arrest. To that end, sublines of Rat1 fibroblasts capa

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Bolner, Michelle, Pamela Fink, and Ellen Richie. "The absence of thymus involution in K5.Cyclin D1 transgenic mice sustains the output of recent thymic emigrants during aging. (LYM7P.717)." Journal of Immunology 192, no. 1_Supplement (2014): 193.5. http://dx.doi.org/10.4049/jimmunol.192.supp.193.5.

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Abstract Naïve T cells are continually exported from the thymus and maintain peripheral TCR repertoire diversity. As the thymus involutes with age, thymopoiesis and T cell output wane, reducing the number of recent thymic emigrants (RTEs). Although homeostatic proliferation of memory T cells sustains peripheral T cell numbers, the decrease in naïve T cells restricts immune responsiveness to new antigens. It has been proposed that RTE output would be sustained if thymus involution were prevented. To test this hypothesis, we analyzed RTEs in mice that do not undergo thymus involution due to a ke

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Lin, Shankung, Wengong Wang, Gerald M. Wilson, et al. "Down-Regulation of Cyclin D1 Expression by Prostaglandin A2 Is Mediated by Enhanced Cyclin D1 mRNA Turnover." Molecular and Cellular Biology 20, no. 21 (2000): 7903–13. http://dx.doi.org/10.1128/mcb.20.21.7903-7913.2000.

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ABSTRACT Prostaglandin A2 (PGA2), an experimental chemotherapeutic agent, causes growth arrest associated with decreased cyclin D1 expression in several cancer cell lines. Here, using human non-small-cell lung carcinoma H1299 cells, we investigated the mechanisms whereby PGA2 down-regulates cyclin D1 expression. Transcription rates of the cyclin D1 gene, studied using a cyclin D1 promoter-luciferase construct and nuclear run-on assays, were not affected by PGA2 treatment. Instead, the cyclin D1 mRNA was rendered unstable after exposure to PGA2. Since the stability of labile mRNA is modulated t

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Ujie, Michiko, Kosuke Takada, Maki Kiso, et al. "Long-term culture of human lung adenocarcinoma A549 cells enhances the replication of human influenza A viruses." Journal of General Virology 100, no. 10 (2019): 1345–49. http://dx.doi.org/10.1099/jgv.0.001314.

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Long-term culture of the human lung adenocarcinoma cell line A549 promotes the differentiation of these cells toward an alveolar type II cell phenotype. Here, we evaluated the susceptibility of long-term cultured A549 cells to human influenza viruses. A549 cells were cultured continuously for 25 days (D25-A549) or 1 day (D1-A549) in Ham’s F12K medium. Six human influenza A viruses grew much faster in D25-A549 cells than in D1-A549 cells; however, two influenza B viruses replicated poorly in both cell types. Two avian influenza viruses replicated efficiently in both cell types, with similar tit

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Nickerson, Helen D., Marta Chesi, and Peter Leif Bergsagel. "Myeloma Cell Lines Are Not Sensitive to Modulation of Cyclin D1 Level." Blood 104, no. 11 (2004): 790. http://dx.doi.org/10.1182/blood.v104.11.790.790.

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Abstract Dysregulation of D type cyclins is an almost universal event in multiple myeloma. Overexpression of cyclin D1 may occur by chromosomal translocation of t(11:14)(q13:32), and also in association with hyperdiploidy. To investigate the role of cyclin D1 in the growth of human myeloma cell lines, we used both shRNA plasmid constructs, and an siRNA Smartpool against cyclin D1 and compared to control cells transfected with anti-GFP or GAPDH constructs. siRNA was electroporated into multiple myeloma cell lines overexpressing cyclin D1 (KMS12PE, U266, H929) which gave a 50–60% transfection ef

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Roue, Gael, Vianney Pichereau, Hubert Lincet, Xavier Troussard, and Brigitte Sola. "Cyclin D1 Mediates Resistance towards p53-Independent and -Dependent Apoptosis through Anti-Apoptotic Factors and Molecular Chaperones." Blood 106, no. 11 (2005): 4294. http://dx.doi.org/10.1182/blood.v106.11.4294.4294.

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Abstract Cyclin D1 is a key regulator of the G1 to S transition of the cell cycle, physiologically absent in normal lymphocytes, but overexpressed in some lymphoproliferative disorders such as mantle cell lymphoma or multiple myeloma. While cyclin D1 has also been shown to control other aspects of the cellular fate, such as cellular senescence, apoptosis or tumorigenesis, its precise role in the pathogenesis of B-cell lymphomas and leukemias is still unclear. In this context, using various cell lines derived from the pre-B murine cell line BaF3 and conditionally expressing cyclin D1, we have p

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Sewing, A., C. Burger, S. Brusselbach, C. Schalk, F. C. Lucibello, and R. Muller. "Human cyclin D1 encodes a labile nuclear protein whose synthesis is directly induced by growth factors and suppressed by cyclic AMP." Journal of Cell Science 104, no. 2 (1993): 545–55. http://dx.doi.org/10.1242/jcs.104.2.545.

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We show that the cyclin D1 gene is regulated by a variety of growth factors in human diploid fibroblasts (WI-38). Expression of cyclin D1 mRNA is low in quiescent WI-38 cells and reaches a maximum around 10 hours after serum stimulation, i.e. approximately 8 hours prior to the onset of DNA synthesis. A cyclin D1-specific antiserum raised against a bacterially expressed fusion protein detected a 39 kDa polypeptide in WI-38 cells. In agreement with the RNA expression data, cyclin D1 protein synthesis is also serum-inducible, reaching a maximum around 9 hours post-stimulation. The results obtaine

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Beltran, Elena, Vicente Fresquet, Javier Martinez-Useros, et al. "A Novel Pro-Survival Function of Cyclin-D1 Underlies Its Oncogenic Role and Potential as a Therapeutic Target In Mantle Cell Lymphoma." Blood 116, no. 21 (2010): 769. http://dx.doi.org/10.1182/blood.v116.21.769.769.

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Abstract Abstract 769 Despite the many and diverse therapeutic approaches used to treat patients with mantle cell lymphoma (MCL), it remains an incurable disease. Recently, attention has turned into novel therapies targeting MCL-specific oncogenic pathways important for the growth and maintenance of the transformed phenotype. The chromosomal translocation t(11;14)(q13;q32) leading to cyclin-D1 over-expression is the hallmark of MCL. Constitute cyclin-D1 activation in B-lymphocytes maintains retinoblastoma protein in a phosphorylated state and promotes cell cycling, thus initiating the tumorige

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Xu, Yi, Xin Sun, Jing Chen, Jinbiao Xu, and Junshui Wei. "Knockdown of lncRNA ENST00000603829 Inhibits the Proliferation and Invasion of Salivary Gland Pleomorphic Adenoma through Regulating Cyclin D1." Applied Bionics and Biomechanics 2022 (April 27, 2022): 1–11. http://dx.doi.org/10.1155/2022/8805305.

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Objective. Salivary gland pleomorphic adenoma (SPA) is a benign neoplasm that can still recur even after radical surgery. To investigate its underlying pathogenesis, here, we examined the significance of lncRNA ENST00000603829 in the proliferation and invasion of SPA. Methods. SPA tissues ( n = 30 ) and adjacent normal tissues (NC; n = 30 ) were collected from SPA patients treated at our hospital from June 2017 to December 2019. The human normal salivary gland epithelial cell line (HSG) and SPA cells (PA30, PA37, and PA116) were cultured. qRT-PCR was used for detecting the expression of cyclin

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Ott, M. Michaela, Jirina Bartkova, Jiri Bartek, et al. "Cyclin D1 Expression in Mantle Cell Lymphoma Is Accompanied by Downregulation of Cyclin D3 and Is Not Related to the Proliferative Activity." Blood 90, no. 8 (1997): 3154–59. http://dx.doi.org/10.1182/blood.v90.8.3154.

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Abstract The cell cycle regulatory protein cyclin D1 is essential for G1-S phase transition in several epithelial and mesenchymal tissues but is apparently not essential in normal mature B cells. An overexpression of cyclin D1 is induced by the chromosomal translocation t(11; 14)(q13; q32), which characterizes non-Hodgkin's lymphomas (NHLs) of mantle cell type. We studied 26 cases of mantle cell lymphoma (MCL) for the expression of cyclins D1 and D3. A total of 23 lymphomas showed a nuclear staining for cyclin D1, whereas reactive B cells of residual germinal centers were constantly negative.

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Morita, Kenji. "Differential cortical activation of the striatal direct and indirect pathway cells: reconciling the anatomical and optogenetic results by using a computational method." Journal of Neurophysiology 112, no. 1 (2014): 120–46. http://dx.doi.org/10.1152/jn.00625.2013.

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The corticostriatal system is considered to be crucially involved in learning and action selection. Anatomical studies have shown that two types of corticostriatal neurons, intratelencephalic (IT) and pyramidal tract (PT) cells, preferentially project to dopamine D1 or D2 receptor-expressing striatal projection neurons, respectively. In contrast, an optogenetic study has shown that stimulation of IT axons evokes comparable responses in D1 and D2 cells and that stimulation of PT axons evokes larger responses in D1 cells. Since the optogenetic study applied brief stimulation only, however, the o

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Jiajia, Dong, Zhang Mingke, Liao Zenglin та ін. "Resolvin-D1 inhibits interleukin-8 and hydrogen peroxide production induced by cigarette smoke extract in 16HBE cells via attenuating NF-κB activation". Chinese Medical Journal 127, № 3 (2014): 511–17. http://dx.doi.org/10.3760/cma.j.issn.0366-6999.20131674.

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Background Cigarette smoke induced airway inflammation plays a role in pathogenesis of airway inflammation. Resolvin-D1 derived from omega-3 polyunsaturated fatty acids is an endogenous anti-inflammatory and proresolving lipid mediator. Resolvin-D1 ameliorated inflammatory responses in lung injury, asthma, peritonitis and atherosclerosis. We investigated whether resolvin-D1 suppressed the productions of chemokines and oxidative stress induced by cigarette smoke extract (CSE) in vitro and its possible mechanism. Methods We examined the proinflammatory chemokine interleukin-8 and hydrogen peroxi

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Saitoh, Maki, Masahide Ohmichi, Kazuhiro Takahashi та ін. "Medroxyprogesterone Acetate Induces Cell Proliferation through Up-Regulation of Cyclin D1 Expression via Phosphatidylinositol 3-Kinase/Akt/Nuclear Factor-κB Cascade in Human Breast Cancer Cells". Endocrinology 146, № 11 (2005): 4917–25. http://dx.doi.org/10.1210/en.2004-1535.

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The mechanism of medroxyprogesterone acetate (MPA)-induced cell proliferation in human breast cancer cells remains elusive. We examined the mechanism by which MPA affects the cyclin D1 expression in progesterone receptor (PR)-positive T47D human breast cancer cells. MPA (10 nm) treatment for 48 h induced proliferation of the cells (1.6-fold induction). MPA induced cyclin D1 expression (3.3-fold induction), and RU486, a selective PR antagonist, blocked the MPA-induced cell proliferation and cyclin D1 expression (23% inhibition). MPA increased both the protein level (2.2-fold induction) and prom

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Li, Zhiping, Chenguang Wang, Xuanmao Jiao, et al. "Cyclin D1 Regulates Cellular Migration through the Inhibition of Thrombospondin 1 and ROCK Signaling." Molecular and Cellular Biology 26, no. 11 (2006): 4240–56. http://dx.doi.org/10.1128/mcb.02124-05.

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ABSTRACT Cyclin D1 is overexpressed in human tumors, correlating with cellular metastasis, and is induced by activating Rho GTPases. Herein, cyclin D1-deficient mouse embryo fibroblasts (MEFs) exhibited increased adhesion and decreased motility compared with wild-type MEFs. Retroviral transduction of cyclin D1 reversed these phenotypes. Mutational analysis of cyclin D1 demonstrated that its effects on cellular adhesion and migration were independent of the pRb and p160 coactivator binding domains. Genomewide expression arrays identified a subset of genes regulated by cyclin D1, including Rho-a

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Hamanaka, Robert B., Beth S. Bennett, Sara B. Cullinan та J. Alan Diehl. "PERK and GCN2 Contribute to eIF2α Phosphorylation and Cell Cycle Arrest after Activation of the Unfolded Protein Response Pathway". Molecular Biology of the Cell 16, № 12 (2005): 5493–501. http://dx.doi.org/10.1091/mbc.e05-03-0268.

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Exposure of cells to endoplasmic reticulum (ER) stress leads to activation of PKR-like ER kinase (PERK), eukaryotic translation initiation factor 2α (eIF2α) phosphorylation, repression of cyclin D1 translation, and subsequent cell cycle arrest in G1phase. However, whether PERK is solely responsible for regulating cyclin D1 accumulation after unfolded protein response pathway (UPR) activation has not been assessed. Herein, we demonstrate that repression of cyclin D1 translation after UPR activation occurs independently of PERK, but it remains dependent on eIF2α phosphorylation. Although phospho

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Schuurhuis, Danita H., Sandra Laban, René E. M. Toes, et al. "Immature Dendritic Cells Acquire Cd8+Cytotoxic T Lymphocyte Priming Capacity upon Activation by T Helper Cell–Independent or–Dependent Stimuli." Journal of Experimental Medicine 192, no. 1 (2000): 145–50. http://dx.doi.org/10.1084/jem.192.1.145.

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The well defined, immature murine dendritic cell (DC) line D1 was used to study the role of DC maturation in CTL induction in vitro and in vivo. Maturation of D1 cells, characterized by markedly increased expression of MHC and costimulatory molecules, was induced by incubation with lipopolysaccharide, agonistic CD40 antibody, or specific CD4+ T helper (Th) cells. Activated, but not immature, D1 cells efficiently primed alloreactive T cell responses in vitro. Similarly, priming of CTL immunity in vivo in CD4-depleted mice was only observed if these mice were immunized with activated D1 cells. T

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Baur, A., K. Bauer, H. Jarry, and J. Kohrle. "Effects of proinflammatory cytokines on anterior pituitary 5'-deiodinase type I and type II." Journal of Endocrinology 167, no. 3 (2000): 505–15. http://dx.doi.org/10.1677/joe.0.1670505.

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Cytokines are locally produced in the anterior pituitary and act through para-/autocrine mechanisms to modulate cell growth and hormone production. 5'-Deiodinases type I (D1) and type II (D2) are also expressed in the anterior pituitary and play an integrative role in the regulation of hormone production and pituitary feedback. D1 activity is known to be regulated by proinflammatory cytokines in liver and thyroid. Therefore, we examined the effects of IL-1 beta, IL-6 and TNF alpha on 5'-deiodinase activities in reaggregates of rat anterior pituitaries and rat somatomammotroph GH3 cells culture

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