Disease relevance of Gcom1

• Modeling mutations in the G1 arrest pathway in human gliomas: overexpression of CDK4 but not loss of INK4a-ARF induces hyperploidy in cultured mouse astrocytes [1].
• Exposure of colorectal cancer (CRC) cells to ionizing radiation results in a cell-cycle arrest in G1 and G2 [2].
• Furthermore, growth comparison of the AsPC-1 adenocarcinoma revealed that, except in the juvenile gland that was morphologically consistent with grade 1 (G1) carcinoma in situ, the number of PCAA-positively stained cells decreased from G1 to grade 4 epithelial differentiation [3].
• TPA-treated MCF-7 cells demonstrated a modest cytostatic response associated with a G1 arrest that was accompanied by Cip1 expression and retinoblastoma hypophosphorylation [4].
• IMPLICATIONS: While the postirradiation increase in G2-phase arrest in cells from breast cancer patients observed in this study may indicate genetic heterozygosity for ataxia-telangiectasia, it might also reflect other genetic abnormalities important to breast cancer [5].

Psychiatry related information on Gcom1

• Moreover, a critical period necessary for histone mRNA accumulation occurred late in G1 phase [6].
• In 2 patients with Alzheimer's disease and 1 with senile dementia an abnormal ganglioside pattern was observed, i.e., a decrease of G1 and G3 in association with an increase of G2 [7].
• G2 aggressive behavior as an adolescent and G3 aggressive behavior as a child were related to parenting behavior but not directly to one another [8].
• An intergenerational, life course model of development identified significant characteristics and events associated with G-2 outcome (education, physical and mental health, healthy lifestyle, and financial independence of public support, emphasizing educational attainment of a high school diploma or a graduate equivalency degree) [9].
• A number of other factors, including parental socioeconomic status (SES), antisocial behavior, depression and Post-traumatic Stress Disorder (PTSD), consistency of discipline, and the perceived early difficulty of the G2 children were measured [10].

High impact information on Gcom1

• Finally, PP1 promotes the exit from mitosis and maintains cells in the G1 or G2 phases of the cell cycle [11].
• An unrelated protein (p19ARF) arises in major part from an alternative reading frame of the mouse INK4a gene, and its ectopic expression in the nucleus of rodent fibroblasts induces G1 and G2 phase arrest [12].
• The nuclear membrane prevents replication of human G2 nuclei but not G1 nuclei in Xenopus egg extract [13].
• Here we show that subsequent attenuation of the PI(3)K/PKB pathway is required to allow transcriptional activation of FKH-TF in G2 [14].
• Reduced levels of p53 correlated with increased G2/M phase arrest, micronucleation, and p53-independent paclitaxel-induced apoptosis [15].

Chemical compound and disease context of Gcom1

• Suspension-cultured mouse plasmacytoma cells (MPC-11) were accumulated in the late G1 phase by exposure to isoleucine-deficient medium for 20-24 h [16].
• The anomalous, calcium-dependent melanoma line (MM170) showed an immediate increase in the thymidine pool size and in nucleoside incorporation and subsequently accumulated in G1 and G2 with diminution of membrane potential and of DNA and RNA synthesis [17].
• The G1 cyclin gene CcnD3, which encodes cyclin D3, is inhibited by dexamethasone in P1798 murine T lymphoma cells [18].
• Cells in G1 phase were preferentially affected by 5-azacytidine, nitrogen mustard, and hyperthermia [19].
• U87MG human glioma cells containing an inducible Akt expression construct were incubated with inducing agent or vehicle, after which the cells were exposed to temozolomide and assayed for activation of the components of the G2 arrest pathway and survival [20].

Biological context of Gcom1

• Sequencing of genomic DNA and cloned transcripts from the 200-kb human GRINL1A gene on chromosome 15 revealed a complex gene structure comprising at least 28 exons [21].
• Loss of normal p53 function confers sensitization to Taxol by increasing G2/M arrest and apoptosis [15].
• The third restriction point occurs in the G2 phase, 2-4 h before mitosis, and is controlled by beta-type growth factors probably produced by helper T lymphocytes [22].
• The second is observed approximately 4 h after mitosis in the G1 phase of the cycle, that is, before DNA replication, and is controlled by growth factors that are produced by macrophages which we have previously classified as alpha-type factors [22].
• In all eukaryotic organisms, inappropriate firing of replication origins during the G2 phase of the cell cycle is suppressed by cyclin-dependent kinases [23].

Anatomical context of Gcom1

• The ability of the two parasites to infect HeLa cells increased as the HeLa cells proceeded from the G1 phase to the S phase of their growth cycle and decreased as the cells entered G2-M [24].
• Here, we describe a cap-independent internal ribosome entry site (IRES) in the ODC mRNA that functions exclusively at G2/M [25].
• Comparison with previous G2-phase arrest data for ataxia-telangiectasia heterozygotes using a cutoff point at 29% delay demonstrated that 20% and 8% of the breast cancer cell lines of the case patients and control subjects, respectively, fell into that category (P < .001) [5].
• Two G1-specific T cell hybridomas exclusively responded to peptide G5 [26].
• Moreover, the presence of KS on G1 can inhibit arthritis development by suppressing T and B cell epitope recognition [26].

Associations of Gcom1 with chemical compounds

• Notably, cells expressing a phosphorylation mutant of PSMA7(Y153F) display impaired G1/S transition and S/G2 progression, highlighting the biological significance of tyrosine phosphorylation of a proteasome subunit as an important cellular regulatory control [27].
• These results indicate that the major aggrecan fragments present in both osteoarthritic human synovial fluid and in normal bovine synovial fluid are large, being composed of a short NH2-terminal stretch of the interglobular domain, the G2 domain, the keratan sulfate domain, and variable lengths of the chondroitin sulfate domain(s) [28].
• When cells released from nocodazole-induced cell cycle arrest were exposed to 200 nM L86-8275, they completed mitosis but arrested in G1 [29].
• Thus rubidazone induced a G2-block, the magnitude and duration of which were dependent on concentration and incubation time [30].
• Both SB 203580 and DN-JNK 1/2 inhibited the acid-induced progression from G0/G1 to G2/M [31].

Analytical, diagnostic and therapeutic context of Gcom1

• Furthermore, an adverse response to radiotherapy was observed in a group of patients with high G2 arrest [5].
• Immunoprecipitation with monoclonal antibodies showed that heterodimerization occurred rapidly, probably in the ER, between newly made G1 and mature, dimerization competent G2 [32].
• A fraction of E-MAP-115 from HeLa cells released from a block at the G1/S boundary runs with higher apparent molecular weight on SDS-PAGE, with a peak correlating with the maximal number of cells in early stages of mitosis [33].
• Microinjection of anti-cdc25A antibodies into G1 cells blocks entry into S phase [34].
• Chromatin immunoprecipitation assays revealed binding of both LIN-9 and B-MYB to the promoters of G2/M regulated genes [35].

References