Assignment of two human cell cycle genes, CDC25C and CCNB1, to 5q31 and 5q12, respectively

Sartor, Heino; Ehlert, F; Grzeschik, Karl‐Heinz; Müller, Rolf; Adolph, Sabine

doi:10.1016/0888-7543(92)90190-4

Cited by 44 publications

(37 citation statements)

References 6 publications

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“…2; Melki et al, 1994;Lefebvre et al, 1995). Typing of STSs for NAIP exon 5 (data not shown), SMN (data not shown), and CCNB1 are consistent with previously reported map positions for these genes and demonstrate that our YACs have not rearranged (Milatovich and Francke, 1992;Sartor et al, 1992;Lefebvre et al, 1995;van der Steege et al, 1995a;Roy et al, 1995;von Deimling et al, 1999). OCLN and CDK7 map to distinct positions centromeric to the SMA inverted duplication.…”

Section: Comparative Gene Mapping Of the Mouse And Humansupporting

confidence: 90%

Evolutionary Divergence of the Mouse and Human Lgn1/SMA Repeat Structures

et al. 2000

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Section: Comparative Gene Mapping Of the Mouse And Humansupporting

confidence: 90%

Evolutionary Divergence of the Mouse and Human Lgn1/SMA Repeat Structures

et al. 2000

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“…The 1.5 Mb CDR in del(5q) contains 2 dual specificity phosphatases that are complimentary coregulators of the G 2 -M checkpoint, i.e., the cell division cycle 25 C (Cdc25C) and the catalytic subunit alpha isoform (PP2Ac␣) and its regulatory subunit B (beta isoform PR 52) of the protein phosphatase 2A (PP2A) (17,18). Cyclin-B/cyclin-dependent kinase-1 (CDK-1, or cdc2) complexes are normally inhibited until G 2 -M entry by phosphorylation of tyrosine (Tyr 15 ) and threonine (Thr 14 ) residues within the ATP binding domain of CDK-1(cdc-2).…”

Section: Haplodeficiency Of the Cdc25c And Pp2aca Phosphatases In Delmentioning

confidence: 99%

A critical role for phosphatase haplodeficiency in the selective suppression of deletion 5q MDS by lenalidomide

Wei

Chen

Rocha

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

181

149

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Fig. 1. Apoptosis induction by lenalidomide is specific for 5q-deleted cells. (A) Cells from AML that evolved from MDS patients with (Center) or without (del) 5q and U937 cells (Left and Right) were exposed to lenalidomide, thalidomide, or vehicle (DMSO) at the concentrations indicated for 48 h before apoptosis was assessed by flow cytometry using Annexin-V/PI staining. Representative results are shown as the mean of the triplicate measurement ± SD from 1 patient. A total of 5 different MDS patients were tested. (B) Lenalidomide arrests 5q deleted cells in G 2 . Cells were treated with lenalidomide at the concentration of 1 μM for 48 h at 37°C and stained with propidium Iodide (PI) in BD Stain Buffer (10 6 /ml) before analysis on BD FACScan. (C) FISH analysis of haplo-deficiency of Cdc25C in (del)5q cells. A normal chromosome 5 showing FISH signals for D5S23/D5S721 (green) and Cdc25C (orange); the ideogram demonstrates the relative gene locations of EGR1 and Cdc25C in 5q31. Probes for EGR1 are commonly used to detect classical 5q deletions. The Right Inset illustrates D5S23/D5S721 and Cdc25C signal pattern for classical 5q deletions in interphase nuclei. (D) Reduced expression of Cdc25C and PP2Acα in bone marrow cells from patients with (del)5q by Q-PCR. RNA was purified from BM-MNC from patients with or without (del)5q as indicated. Relative expression levels of Cdc25C and PP2Acα were analyzed by Q-PCR to quantitate transcript level. Expression is normalized to the reference gene (GAPDH) and fold changes for Cdc25C and PP2Acα in patients are compared with the average data from non(del)5q cells (P < 0.001).

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“…Cell cycle-associated genes developed by the stretch force were directly related to the change of the cell cycle 29) . It controls G2/M checkpoint and contributes to the switch-like, allor-nothing behavior of the cell in deciding to commit to mitosis 30) .…”

Section: Discussionmentioning

confidence: 99%

Effect of Compression Force on Apoptosis in Human Periodontal Ligament Cells

Funakoshi

Yamaguchi

Asano

et al. 2013

J. Hard Tissue Biology.

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The effect of compression force on periodontal ligament (PDL) plays a critical role in orthodontic tooth movement. However, little is known about this effect on apoptosis and the underlying reactive mechanisms in PDL cells. This study focuses on the application of compression force associated with reactive oxygen species (ROS)-induced apoptosis in PDL cells. Following the application of orthodontic force to maxillary first molars, the molars were investigated using immunohistochemical analysis. The cell cycle and apoptosis were assessed in compression force-treated PDL cells using flow cytometry. Furthermore, we assayed the effect on ROS generation by DCFDA fluorescence. In vivo study revealed an increased number of terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) and caspase 8-positive cells in the orthodontic force group. In our in vitro study model, the compression force increased the G1 phase and apoptotic cells. A large increase in the intracellular ROS levels in human (h) PDL cells was observed in the compression force group. Taken together, these results provide new information on compression force-induced G1 arrest and apoptosis in hPDL cells.

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Assignment of two human cell cycle genes, CDC25C and CCNB1, to 5q31 and 5q12, respectively

Cited by 44 publications

References 6 publications

Evolutionary Divergence of the Mouse and Human Lgn1/SMA Repeat Structures

Evolutionary Divergence of the Mouse and Human Lgn1/SMA Repeat Structures

A critical role for phosphatase haplodeficiency in the selective suppression of deletion 5q MDS by lenalidomide

Effect of Compression Force on Apoptosis in Human Periodontal Ligament Cells

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