Disease relevance of CCPG1

• Cell cycle progression in Caulobacter is driven by the master transcriptional regulators CtrA and GcrA [1].
• Cell cycle progression of B-chronic lymphocytic leukemia cells induced to differentiate by TPA [2].
• Cell-cycle progression and apoptosis in K562 and Molt-4 cells after cell-to-cell transmission of HTLV-I: modulation by interferons [3].
• Cell cycle progression during cytomegalovirus infection was investigated by fluorescence-activated cell sorter (FACS) analysis of the DNA content in growth-arrested as well as serum-stimulated human fibroblasts [4].
• Cell cycle progression was studied by flow cytometric analysis, [3H]thymidine incorporation, and phosphorylation of the retinoblastoma gene product, pRB [5].

Psychiatry related information on CCPG1

• Cell cycle progression towards Alzheimer's disease [6].

High impact information on CCPG1

• Cell cycle progression initiated by interleukin-2 (IL-2) in T cells is critical for lymphoproliferation and an immune response [7].
• Cell cycle progression, phosphorylation, and DNA binding of cell cycle checkpoint proteins were analyzed [8].
• Cell cycle progression and de novo centriole assembly after centrosomal removal in untransformed human cells [9].
• Cell cycle progression in eukaryotes is mediated by phosphorylation of protein substrates by the cyclin-dependent kinases (CDKs) [10].
• Cell cycle progression is driven by waves of cyclin expression coupled with regulated protein degradation [11].

Biological context of CCPG1

• Cell cycle progression is monitored by checkpoint mechanisms that ensure faithful duplication and accurate segregation of the genome [12].
• RNA Interference-Mediated Silencing of Mitotic Kinesin KIF14 Disrupts Cell Cycle Progression and Induces Cytokinesis Failure [13].
• Cell cycle progression and chromosome segregation in mammalian cells cultured in the presence of the topoisomerase II inhibitors ICRF-187 [(+)-1,2-bis(3,5-dioxopiperazinyl-1-yl)propane; ADR-529] and ICRF-159 (Razoxane) [14].
• Cell cycle progression proteins (cyclins), oncogene expression, and signal transduction during the proliferative response of human hepatocytes to hepatocyte growth factor [15].
• Cell cycle progression in Caulobacter is governed by a multilayered regulatory network linking chromosome replication with polar morphogenesis and cell division [16].

Anatomical context of CCPG1

• Cell cycle progression in the zygote is identified as a likely precondition for its morphological transition to the ookinete and for the successful establishment of a malaria infection in the mosquito [17].
• Cell-cycle progression of the epithelial cells presenting luminal phenotype was induced only by sequential stimulation/pretreatment with estradiol followed by EGF treatment; this progression was enhanced when estradiol was maintained during EGF treatment [18].
• Cell cycle progression in eukaryotic cells is regulated by a family of cyclin-dependent kinases (CDKs) [19].
• Cell-cycle progression during continuous low dose rate irradiation of a human bladder carcinoma cell line [20].
• Cell cycle progression of synchronized HeLa cells was studied by measuring labeling of the nuclei with [3H]thymidine [21].

Associations of CCPG1 with chemical compounds

• Cell cycle progression for postembryonic cells requires the activity of 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMG-R), the enzyme which catalyzes the production of the isoprenoid precursor, mevalonate [22].
• Cell cycle progression in the presence of high glucose was blocked by tolrestat, which induced a G0-G1 phase growth arrest [23].
• Cell cycle progression of glutathione-depleted human peripheral blood mononuclear cells is inhibited at S phase [24].
• Interference with 3',5'-Cyclic Adenosine Monophosphate Response Element Binding Protein Stimulates Apoptosis through Aberrant Cell Cycle Progression and Checkpoint Activation [25].
• Cell cycle progression in mammalian cells is strictly regulated by both integrin-mediated adhesion to the extracellular matrix and by binding of growth factors to their receptors [26].

Physical interactions of CCPG1

• Cell cycle progression in eukaryotes is controlled by complexes of p34 protein kinases and cyclins [27].

Regulatory relationships of CCPG1

• Cell cycle progression is regulated by cyclin-dependent kinases [28].
• Cell cycle progression requires activation of different cyclin-dependent kinases (CDKs) which are positively regulated by cyclins and negatively regulated by CDK inhibitors [29].
• Cell cycle progression in mammalian cells is regulated by a family of cyclin-dependent kinases (cdks) that are activated by a family of 3 cdc25 phosphatases: cdc25A, cdc25B and cdc25C [30].

Other interactions of CCPG1

• Cell cycle progression is regulated by the combined action of cyclins, cyclin-dependent kinases (CDKs), and CDK inhibitors (CDKIs). p27KIP1, which has a high degree of similarity with p21WAF1, is a general CDKI thought to be involved in G1 arrest in response to agents that inhibit cell cycle progression [31].
• Cell cycle progression is driven by cyclin-dependent kinases, which are positively regulated by association with cyclins and negatively regulated by binding to inhibitory subunits [32].
• Cell-cycle progression is not essential for c-Myc to block differentiation [33].
• Cell cycle progression and induction of apoptosis were assessed by flow cytometry and immunoblot analysis of PARP-cleavage [34].
• Cell cycle progression is regulated by a wide variety of external factors, amongst them are growth factors and extracellular matrix factors [35].

Analytical, diagnostic and therapeutic context of CCPG1

• Cell cycle progression was studied by flow cytometry during one duplication cycle of recipient cells and transcription of HTLV-I was evaluated during the same time course [3].
• Cell cycle progression analyses showed that CTag cells displayed a stronger S phase delay than transformed fibroblasts from normal individuals (IDH4) after treatment with only 2 J/m(2) UVC [36].
• Cell cycle progression was evaluated by immunofluorescence detection and flow cytometric analysis of the proliferating cell nuclear antigen (PCNA) [37].
• Cell cycle progression was determined by flow cytometry, and apoptosis was evaluated by DNA fragmentation. hTERT mRNA levels were quantified by real-time RT-PCR [38].

References