Phosphorus-doped graphitic carbon nitrides (P-g-CN) have recently emerged as promising visible-light photocatalysts for both hydrogen generation and clean environment applications because of fast charge carrier transfer and increased light absorption. However, their photocatalytic performances on CO reduction have gained little attention. In this work, phosphorus-doped g-CN nanotubes are synthesized through the one-step thermal reaction of melamine and sodium hypophosphite monohydrate (NaHPO·HO). The phosphine gas generated from the thermal decomposition of NaHPO·HO induces the formation of P-g-CN nanotubes from g-CN nanosheets, leads to an enlarged BET surface area and a unique mesoporous structure, and creates an amino-rich surface. The interstitial doping phosphorus also down shifts the conduction and valence band positions and narrows the band gap of g-CN. The photocatalytic activities are dramatically enhanced in the reduction both of CO to produce CO and CH and of water to produce H because of the efficient suppression of the recombination of electrons and holes. The CO adsorption capacity is improved to 3.14 times, and the production of CO and CH from CO increases to 3.10 and 13.92 times that on g-CN, respectively. The total evolution ratio of CO/CH dramatically decreases to 1.30 from 6.02 for g-CN, indicating a higher selectivity of CH product on P-g-CN, which is likely ascribed to the unique nanotubes structure and amino-rich surface.

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Plant organ size shows remarkable uniformity within species indicating strong endogenous control. We have identified a plant growth regulatory gene, functionally and structurally homologous to human EBP1. Plant EBP1 levels are tightly regulated; gene expression is highest in developing organs and correlates with genes involved in ribosome biogenesis and function. EBP1 protein is stabilised by auxin. Elevating or decreasing EBP1 levels in transgenic plants results in a dose-dependent increase or reduction in organ growth, respectively. During early stages of organ development, EBP1 promotes cell proliferation, influences cell-size threshold for division and shortens the period of meristematic activity. In postmitotic cells, it enhances cell expansion. EBP1 is required for expression of cell cycle genes; CyclinD3;1, ribonucleotide reductase 2 and the cyclin-dependent kinase B1;1. The regulation of these genes by EBP1 is dose and auxin dependent and might rely on the effect of EBP1 to reduce RBR1 protein level. We argue that EBP1 is a conserved, dose-dependent regulator of cell growth that is connected to meristematic competence and cell proliferation via regulation of RBR1 level.

Ebp1, an ErbB-3 binding protein, inhibits the proliferation and induces the differentiation of human breast cancer cells. The mechanisms of these effects are unknown. Rb, the product of the retinoblastoma gene, is an important modulator of cell cycle progression and cellular differentiation. We report that Rb is a binding target for Ebp1. Ebp1 was localized to both the nucleus and the cytoplasm of logarithmically growing AU565 breast cancer cells and HeLa cells as determined by confocal immunofluorescent microscopy. Ebp1 was present in Rb immunoprecipitates derived from AU565 breast cancer cells. GST-Rb also bound endogenous Ebp1. Using GST-Ebp1 constructs, we determined that the 72 C-terminal amino acids of Ebp1 were sufficient to bind Rb. Dephosphorylation of Ebp1 enhanced the interaction of Ebp1 with Rb. The overexpression of Ebp1 in MCF-7 and AU565 (Rb(+)) cells inhibited the activity of the E2F1 regulated cyclin-E promoter. Ebp1 bound E2F1 indirectly via Rb in lysates of MCF-7 cells. The interaction of Ebp1 with Rb may prove to be an important mechanism of Ebp1 induced changes in cell proliferation and differentiation.

Down-regulation of the androgen receptor (AR) is being evaluatedas an effective therapy for the advanced stages of prostate cancer. We report that Ebp1, a protein identified by its interactions with the ErbB3 receptor, down-regulates expression of AR and ARregulated genes in the LNCaP prostate cancer cell line. Using microarray analysis, we identified six endogenous AR target genes, including the AR itself, that are down-regulated by ebp1 overexpression. Chromatin immunoprecipitation assays revealed that Ebp1 was recruited to the prostate-specific antigen gene promoter in response to the androgen antagonist bicalutamide, suggesting that Ebp1 directly affected the expression of AR-regulated genes in response to androgen antagonists. Ebp1 expression was reduced in cells that had become androgen-independent. Androgens failed to stimulate either the growth of ebp1 transfectants or transcription of AR-regulated reporter genes in these cells. The agonist activity of the antiandrogen cyproterone acetate was abolished in ebp1 transfectants. In severe combined immunodeficient mice, Ebp1 overexpression resulted in a reduced incidence of LNCaP tumors and slower tumor growth. These findings suggest that Ebp1 is a previously unrecognized therapeutic target for treatment of hormone refractory prostate cancer.ErbB receptors ͉ transcriptional corepressors ͉ androgen independence