Disease relevance of Ccpg1

• Cell cycle progression was blocked at temperatures below 27 degrees C. Immediately after shift to hypothermic temperatures, cells became more sensitive to hyperthermia [1].
• Cell cycle progression of G2 fractions (75-80% G2 (4C) cells) from 8 h anaerobically cultured asynchronous hyperdiploid Ehrlich ascites tumor cells strain Karzel, separated by centrifugal elutriation, was studied after reaeration by flow cytometric methods, including the BrdU-H33258 technique and dual parameter measurements [2].

High impact information on Ccpg1

• Cell cycle progression is monitored by highly coordinated checkpoint machinery, which is activated to induce cell cycle arrest until defects like DNA damage are corrected [3].
• Cell cycle progression and apoptosis after irradiation in an acidic environment [4].
• Cell-cycle progression was monitored by 5-bromo-2-deoxyuridine (BrdU) incorporation into the DNA, the frequency of mitoses, the expression of cell-cycle control genes, and by flow cytometry [5].
• Cell-cycle progression is regulated predominantly by a series of serine/threonine kinases, the cyclin-dependent kinases (CDKs) [6].
• Cell cycle progression of the YAC-1 target was studied by dual parameter analysis of DNA content and bromodeoxyuridine incorporation into tumor cell DNA either prior to or following addition of PMNs [7].

Biological context of Ccpg1

• Cell cycle progression and the effect of the drug on various transition points in the cell cycle (i.e. G1 to S phase, through a window in early S phase and G2 phase to mitosis) were monitored by flow cytometry [8].
• Cell cycle progression of parthenogenetically activated mouse oocytes to interphase is dependent on the level of internal calcium [9].
• Cell-cycle progression is arrested at G1/S, mediated at least partially through the upregulation of the cyclin-dependent kinase inhibitor p27 [10].
• Cell cycle progression of asynchronously grown MPC-11 cells was inhibited by both agents, but, in contrast to the G1 phase arrest caused by TPA, okadaic acid gave rise to G2/M phase and S phase arrest [11].
• Cell cycle progression kinetics of regenerating mouse epidermal cells: an in vivo study combining DNA flow cytometry, cell sorting, and [3H]dThd autoradiography [12].

Anatomical context of Ccpg1

• Cell cycle progression of this cell line is doxycycline-dependent [13].
• Cell cycle progression in photoreceptors could not be demonstrated [14].
• Cell cycle progression of granulosa cells is critical for ovarian function, especially follicular maturation [15].
• Cell cycle progression of C3H 10T1/2 and 3T3 cells in the absence of an increase in c-myc RNA levels [16].
• Cell cycle progression in denV-transfected murine fibroblasts exposed to ultraviolet radiation [17].

Associations of Ccpg1 with chemical compounds

• Cell cycle progression was assessed by saponin/propidium iodide staining and fluorescence-activated cell sorter analysis [18].
• Cell cycle progression was blocked in G(2)/M with 40 and 80 mcmol/L genistein [19].

Other interactions of Ccpg1

• Cell cycle progression is subject to several regulatory controls, of which the p53 protein plays a major role in growth arrest, subsequent to the detection of cellular aberrations [20].
• Cell cycle progression requires that cyclin-dependent kinases be activated by cyclins [21].
• Cell cycle progression into the S phase was accelerated in the c-fos B cells [22].
• Cell cycle progression of mouse macrophage cells was impaired by interferon-gamma (IFN-gamma) [23].
• Cell cycle progression without cyclin E/CDK2: breaking down the walls of dogma [24].

Analytical, diagnostic and therapeutic context of Ccpg1

• Cell cycle progression and the terminal point of action of the drug were monitored by flow cytometry [25].

References