Dual-mode self-powered photoelectrochemical and colorimetric determination of procalcitonin accomplished by multienzyme-expressed Ni4Cu2 bimetallic hollow nanospheres and spherical nanoflower-MoS2/Cu2ZnSnS4/Bi2S3.

Bacterial infections, viral infections and autoimmune diseases pose a considerable threat to human health. Procalcitonin (PCT) has emerged as a biomarker for the detection of these diseases. To ensure accurate and reliable results, we propose a dual-mode approach that incorporates self-validation and self-correction mechanisms. Herein, we develop a dual-mode self-powered photoelectrochemical (PEC) and colorimetric sensor to determine PCT. The self-powered PEC sensor was constructed with a photoanode of spherical nanoflower-MoS2/Cu2ZnSnS4/Bi2S3 material and a photocathode of CuInS2 material. Ni4Cu2 bimetallic hollow nanospheres (BHNs) possess superoxide dismutase and catalase performance, which facilitate superoxide anion radical (·O2-) and H2O2 circulating generation, promoting the separation of photogenerated electrons and holes to amplify photocurrent signal. Thus Ni4Cu2 BHNs is used as a marker material for PEC sensor. Meanwhile, in colorimetric mode, Ni4Cu2 BHNs converts blue oxTMB to a colourless TMB for colorimetric detection of PCT. Based on this principle, dual-mode determination of PCT with high sensitivity is achieved. The dual-mode method not only demonstrates outstanding properties and practicability, but also presents an effective, highly efficient and reliable method for detecting PCT.

Advances in structure-based drug design: The potential for precision therapeutics in psychiatric disorders.

Over the years, the field of GPCR drug design has undergone a remarkable evolution, fueled by advancements in science and technology. This evolution has given rise to a diverse range of ideas and approaches in structure-based drug design, bolstering the versatility and strength of the GPCR drug design toolbox. This review encapsulates the iterative development process, navigating challenges and opportunities in structure-based drug design within GPCRs. With a focused emphasis on its impact on psychiatric disorders, the review accentuates recent advancements and delves into the potentials unlocked by emerging technologies. The review explores the intricate interplay between scientific progress and iterative refinement, offering profound insights into the potential pathways that lie ahead for GPCR drug design.

Nutrient transfer and antioxidant effect of adzuki bean before and after GABA enrichment.

In order to study the nutritional changes of γ-aminobutyric acid (GABA) enrichment in adzuki bean germination, vacuum combined with monosodium glutamate (MSG) was used as the germination stress of adzuki bean. The nutrient transfer before and after GABA enrichment in adzuki bean germination under vacuum combined with MSG stress were studied by means of chromatography and scanning electron microscope (SEM). The antioxidant activity and hypoglycemic effect of different solvent extracts before and after germination of adzuki bean were evaluated by experiments in vitro. The results showed that the nutritional characteristics of adzuki bean rich in GABA changed significantly (P < 0.05), the total fatty acids decreased significantly (P < 0.05), and the 21 amino acids detected increased significantly. After germination, the starch granules of adzuki bean became smaller and the surface was rough Germination stress significantly increased the antioxidant and hypoglycemic activities of the extracts from different solvents (P < 0.05), and the water extracts had the best effect on DPPH and ⋅OH radical scavenging rates of 88.52 and 83.56%, respectively. The results indicated that the germinated adzuki bean rich in GABA was more nutritious than the raw adzuki bean and had good antioxidant activity. It hoped to provide technical reference for rich food containing GABA.

Identification and verification of a 4-gene signature predicting the overall survival of cervical cancer.

Cervical cancer (CC) is one of the most common gynecological malignancies, ranking fourth in both incidence and mortality in women worldwide. Early screening and treatment are of great significance in reducing the incidence and mortality of CC. Due to the complex molecular mechanisms of tumor progression, the predictive power of traditional clinical information is limited. In this study, an effective molecular model is established to assess prognosis of patients with CC and guide clinical treatment so as to improve their survival rate. Three high quality datasets (GSE138080, GSE52904, GSE67522) of expression profiling were obtained from gene expression omnibus (GEO) database. Another mRNA expression and clinicopathological data of CC were obtained from The Cancer Genome Atlas (TCGA) dataset. The bioinformatic analyses such as univariate analysis, multivariate Cox proportional-hazards model (Cox) analysis and lasso regression analysis were conducted to select survival-related differentially expressed genes (DEGs) and further establish a prognostic gene signature. Moreover, the performance of prognostic gene signature was evaluated based on Kaplan-Meier curve and receiver operating characteristic (ROC) curve. Gene set enrichment analysis (GSEA) and tumor immunity analysis were carried out to elucidate the molecular mechanisms and immune relevance. A 4-gene signature comprising procollagen-lysine, 2-oxoglutarate 5-dioxygenase 2 (PLOD2), spondin1 (SPON1), secreted phosphoprotein 1 (SPP1), ribonuclease H2 subunit A (RNASEH2A) was established to predict overall survival (OS) of CC. The ROC curve indicated good performance of the 4-gene signature in predicting OS of CC based on the TCGA dataset. The 4-gene signature classified the patients into high-risk and low-risk groups with distinct OS rates of CC. Univariate analysis and multivariate Cox regression analysis revealed that the 4-gene signature was an independent factor affecting the prognosis of patients with CC. Our study developed a 4-gene signature capable of predicting the OS of CC. The findings may be beneficial to individualized clinical treatment and timely follow-up for patients with CC.

ZBTB20 Regulates Prolactin Expression and Lactotrope Function in Adult Mice.

Lactotropes are prolactin (PRL)-secreting endocrine cells in the anterior pituitary. We have established the zinc finger protein ZBTB20 as an essential transcription factor for lactotrope specification, the disruption of which results in complete loss of lactotropes in mice. However, the potential role of ZBTB20 in mature lactotropes remains unclear. Here we demonstrate that ZBTB20 acts as a critical cell-autonomous regulator for PRL expression in mature lactotropes in adult mice. Via a CRISPR/Cas9 approach, we first generated a tamoxifen-inducible Prl-CreER knockin mouse line that could efficiently mediate gene recombination specifically in lactotropes. Conditional deletion of the Zbtb20 gene specifically in mature lactotropes at adulthood led to a substantial decrease in PRL levels both in the pituitary and in plasma, without significant alterations of lactotrope relative density in the pituitary from male or female mice. Furthermore, conditional disruption of Zbtb20 in adult female mice did not significantly change pregnancy-elicited lactotrope expansion, but caused an impaired mammary gland expansion and lactation due to the PRL defect. Thus, our data point to an important role of ZBTB20 in regulating PRL expression and lactotrope function at adulthood.

Ratiometric electrochemical immunoassay for procalcitonin based on dual signal probes: Ag NPs and Nile blue A.

In order to determine procalcitonin, a sandwich-type ratiometic electrochemical immunosensor was developed by differential pulse voltammetry (DPV). Due to high chemical stability and good biocompatibility, graphitic carbon nitride (g-C3N4) could be used as feasible supporter to carry silver nanoparticles (Ag NPs) with an obvious oxidative peak (measured typically at + 0.3 V vs. SCE). Ag NPs loaded onto g-C3N4 were not only beneficial to prevent the agglomeration of Ag NPs, but also favorable to improve the electron transfer velocity of g-C3N4. Moreover, the g-C3N4-Ag NPs as the matrix could immobilize primary antibody by Ag-N bond. Nile blue A (NBA), an excellent redox probe based on the redox reaction with two-electrons, provides a current signal at - 0.38 V (vs. SCE). Zr-based metal organic framework (UiO-67), an ideal framework material with large specific surface area and high porosity, could absorb the substantial water-soluble NBA by electrostatic adsorption. The UiO-67 modified by NBA (NBA-UiO-67) owned admirable biocompatibility and was a qualifying marker to load the secondary antibody. For the immunosensor, the current ratio of NBA to Ag NPs (INBA/IAg NPs) was increased as the concentrations of PCT increased. Under the optimum conditions, the linear range of the immunosensor was 0.005 to 50 ng/mL; the detection limit was 1.67 pg/mL (S/N = 3), which reflected the excellent analytical performance of the sensor. The proposed immunosensor strategy is a simple and dependable platform, with great application potential in biometric analysis.

Continuous growth phenomenon for direct synthesis of monodisperse water-soluble iron oxide nanoparticles with extraordinarily high relaxivity.

The direct synthesis of highly water-soluble nanoparticles has attracted intensive interest, but systematic size control has not been reported. Here, we developed a general method for synthesizing monodisperse water-soluble iron oxide nanoparticles with nanometer-scale size increments from 4 nm to 13 nm in a single reaction. Precise size control was achieved by continuous growth in an amphiphilic solvent, diethylene glycol (DEG), where the growth step was separated from the nucleation step by sequential addition of a reactant. There was only one reactant in the synthesis and no need for additional capping agents and reducing agents. This study reveals the "living growth" character of iron oxide nanoparticles synthesised in an amphiphilic solvent. The synthetic method shows high reproducibility. The as-prepared iron oxide nanoparticles are extremely water soluble without any surface modification. Surprisingly, the synthesized 9 nm iron oxide nanoparticles exhibit extremely high transversal and longitudinal relaxivities of 425 mM-1 s-1 and 32 mM-1 s-1 respectively, which is among the highest transversal relaxivity in the literature for sub-10 nm spherical nanoparticles. This study will not only shed light on the continuous growth phenomenon of iron oxide nanoparticles in an amphiphilic solvent, but could also stimulate the synthesis and application of iron oxide nanoparticles. The continuous growth method could be further extended to other materials for the controlled synthesis of water-soluble nanoparticles.

Liver ChREBP Protects Against Fructose-Induced Glycogenic Hepatotoxicity by Regulating L-Type Pyruvate Kinase.

Excessive fructose consumption is closely linked to the pathogenesis of metabolic disease. Carbohydrate response element-binding protein (ChREBP) is a transcription factor essential for fructose tolerance in mice. However, the functional significance of liver ChREBP in fructose metabolism remains unclear. Here, we show that liver ChREBP protects mice against fructose-induced hepatotoxicity by regulating liver glycogen metabolism and ATP homeostasis. Liver-specific ablation of ChREBP did not compromise fructose tolerance, but rather caused severe transaminitis and hepatomegaly with massive glycogen overload in mice fed a high-fructose diet, while no obvious inflammation, cell death, or fibrosis was detected in the liver. In addition, liver ATP contents were significantly decreased by ChREBP deficiency in the fed state, which was rendered more pronounced by fructose feeding. Mechanistically, liver contents of glucose-6-phosphate (G6P), an allosteric activator of glycogen synthase, were markedly increased in the absence of liver ChREBP, while fasting-induced glycogen breakdown was not compromised. Furthermore, hepatic overexpression of LPK, a ChREBP target gene in glycolysis, could effectively rescue glycogen overload and ATP reduction, as well as mitigate fructose-induced hepatotoxicity in ChREBP-deficient mice. Taken together, our findings establish a critical role of liver ChREBP in coping with hepatic fructose stress and protecting from hepatotoxicity by regulating LPK.

Response of gas-exchange characteristics and chlorophyll fluorescence to acute sulfur dioxide exposure in landscape plants.

To explore the toxicity and action mechanism of acute sulfur dioxide (SO2) on urban landscape plants, a simulated SO2 stress environment by using fumigation chamber involving increasing SO2 concentration (0, 25, 50, 100, 200 mg m-3) was carried out among three species. After 72 h of exposure, SO2-induced oxidative damage indicated by electrolyte leakage increased with higher dose of SO2. Meanwhile, SO2 decreased the contents of chlorophyll a, chlorophyll b and carotenoid and increased the contents of sulfur. Net photosynthetic rate (Pn) decreased as a result of stomatal closure when SO2 dose was lower than 50 mg m-3, out of this range, non-stomatal limitation play a dominant role in the decline of Pn. Simultaneous measurements of chlorophyll fluorescence imaging (CFI) also revealed that the maximal quantum efficiency of PSII photochemistry in dark-adapted state (Fv/Fm) and the realized operating efficiency of PSII photochemistry (Fq'/Fm') was reduced by SO2 in a dose-dependent manner. In addition, the maximum quantum efficiency of PSII photochemistry in light-adapted state (Fv'/Fm') and the PSII efficiency factor (Fq'/Fv') decreased when exposure to SO2. These results implied that acute SO2 exposure induced photoinhibition of PSII reaction centers in landscape plants. Our study also indicated that different urban landscape plant species resist differently to SO2: Euonymus kiautschovicus > Ligustrum vicaryi > Syringa oblata according to gas-exchange characteristics and chlorophyll fluorescence responses.

Dissection and Coronal Slice Preparation of Developing Mouse Pituitary Gland.

The pituitary gland or hypophysis is an important endocrine organ secreting hormones essential for homeostasis. It consists of two glands with separate embryonic origins and functions - the neurohypophysis and the adenohypophysis. The developing mouse pituitary gland is tiny and delicate with an elongated oval shape. A coronal section is preferred to display both the adenohypophysis and neurohypophysis in a single slice of the mouse pituitary. The goal of this protocol is to achieve proper pituitary coronal sections with well-preserved tissue architectures from developing mice. In this protocol, we describe in detail how to dissect and process pituitary glands properly from developing mice. First, mice are fixed by transcardial perfusion of formaldehyde prior to dissection. Then three different dissecting techniques are applied to obtain intact pituitary glands depending on the age of mice. For fetal mice aged embryonic days (E) 17.5 - 18.5 and neonates up to 4 days, the entire sella regions including the sphenoid bone, gland, and trigeminal nerves are dissected. For pups aged postnatal days (P) 5 - 14, the pituitary glands connected with trigeminal nerves are dissected as a whole. For mice over 3 weeks old, the pituitary glands are carefully dissected free from the surrounding tissues. We also display how to embed the pituitary glands in a proper orientation by using the surrounding tissues as landmarks to obtain satisfying coronal sections. These methods are useful in analyzing histological and developmental features of pituitary glands in developing mice.

miR-21 inhibitor suppresses cell proliferation and colony formation through regulating the PTEN/AKT pathway and improves paclitaxel sensitivity in cervical cancer cells.

The present study aimed to investigate the role and the molecular mechanisms underlying the effects of microRNA-21 (miR-21) on the proliferation, apoptosis and colony formation of cervical cancer cells, and to examine the role of miR-21 in mediating the sensitivity of cervical cancer cells to paclitaxel (PTX). Reverse transcription­quantitative polymerase chain reaction was employed to determine the level of miR­21 in various cervical cancer and normal cervical cells. The results revealed that the expression levels of miR-21 in cervical cancer cells were markedly higher when compared with normal cervical cells. Subsequently, a miR­21 inhibitor or negative control (NC) was transfected into cervical cancer cells. Cell viability, colony formation and apoptosis were then analyzed using an MTT assay, crystal violet and Annexin V-fluorescein isothiocyanate/propidium iodide staining, respectively. The protein expression level of B-cell lymphoma­2 (Bcl­2), Bcl­2­associated X (Bax), programmed cell death 4 (PDCD4), survivin, c­myc, phosphatase and tensin homolog (PTEN) and phosphorylated (p)­AKT were determined by western blot analysis. The sensitivity of cervical cancer cells to PTX (25, 50 and 100 µg/ml) was characterized using an MTT assay. The results demonstrated that the miR-21 inhibitor promoted apoptosis of cervical cancer cells and suppressed their proliferation and colony formation when compared with the NC. In addition, the expression levels of Bcl­2, survivin, c­myc and p­AKT were significantly downregulated in cells transfected with the miR­21 inhibitor, whilst the expression levels of Bax, PDCD4 and PTEN were significantly upregulated. Furthermore, the miR­21 inhibitor significantly enhanced the inhibition efficacy of PTX at a range of concentrations in cervical cancer cells. It was concluded that inhibition of miR­21 suppressed cell proliferation and colony formation through regulating the PTEN/AKT pathway, and improved PTX sensitivity in cervical cancer cells. The results of the present study may contribute to the development of miRNA­based cervical cancer therapy in the future.

ZBTB20 is required for anterior pituitary development and lactotrope specification.

The anterior pituitary harbours five distinct hormone-producing cell types, and their cellular differentiation is a highly regulated and coordinated process. Here we show that ZBTB20 is essential for anterior pituitary development and lactotrope specification in mice. In anterior pituitary, ZBTB20 is highly expressed by all the mature endocrine cell types, and to some less extent by somatolactotropes, the precursors of prolactin (PRL)-producing lactotropes. Disruption of Zbtb20 leads to anterior pituitary hypoplasia, hypopituitary dwarfism and a complete loss of mature lactotropes. In ZBTB20-null mice, although lactotrope lineage commitment is normally initiated, somatolactotropes exhibit profound defects in lineage specification and expansion. Furthermore, endogenous ZBTB20 protein binds to Prl promoter, and its knockdown decreases PRL expression and secretion in a lactotrope cell line MMQ. In addition, ZBTB20 overexpression enhances the transcriptional activity of Prl promoter in vitro. In conclusion, our findings point to ZBTB20 as a critical regulator of anterior pituitary development and lactotrope specification.

Escherichia coli nfuA is essential for maintenance of Shiga toxin phage Min27 lysogeny under iron-depleted condition.

It has been earlier hypothesized that lysogenic infection with Stx-encoding phages influences protein expression in the bacterial host, and therefore, some differentially expressed proteins could affect survival characteristics and pathogenicity. We compared the protein expression profiles of the host MG1655 and lysogens by 2D electrophoresis. Four different genes identified were all related to Fe/S subunit production, namely, nfuA, fdoH, sdhB and ftnA. To explore the role of nfuA in the biology of Stx prophage lysogeny, gene knockout experiments and phage lysogenic conversion were performed. The inactivation of nfuA caused the prophage to enter its lytic life cycle, especially under an iron-depleted condition. A similar activity was also detected in the Escherichia coli O157:H7 strain from which the Stx phage Min 27 was originally isolated. NfuA might be the positive regulator of genes controlling lysogenic cycle such as cI, cII and cIII since their transcriptional level was significantly reduced in nfuA deletion mutant as shown by qRT-PCR. We conclude that NfuA is essential for maintenance of Stx phage lysogeny in host's genetic reservoir under iron-deficient condition.

ZBTB20 is a sequence-specific transcriptional repressor of alpha-fetoprotein gene.

Alpha-fetoprotein (AFP) represents a classical model system to study developmental gene regulation in mammalian cells. We previously reported that liver ZBTB20 is developmentally regulated and plays a central role in AFP postnatal repression. Here we show that ZBTB20 is a sequence-specific transcriptional repressor of AFP. By ELISA-based DNA-protein binding assay and conventional gel shift assay, we successfully identified a ZBTB20-binding site at -104/-86 of mouse AFP gene, flanked by two HNF1 sites and two C/EBP sites in the proximal promoter. Importantly, mutation of the core sequence in this site fully abolished its binding to ZBTB20 in vitro, as well as the repression of AFP promoter activity by ZBTB20. The unique ZBTB20 site was highly conserved in rat and human AFP genes, but absent in albumin genes. These help to explain the autonomous regulation of albumin and AFP genes in the liver after birth. Furthermore, we demonstrated that transcriptional repression of AFP gene by ZBTB20 was liver-specific. ZBTB20 was dispensable for AFP silencing in other tissues outside liver. Our data define a cognate ZBTB20 site in AFP promoter which mediates the postnatal repression of AFP gene in the liver.

The mechanism and significance of synergistic induction of the expression of plasminogen activator inhibitor-1 by glucocorticoid and transforming growth factor beta in human ovarian cancer cells.

Plasminogen activator inhibitor-1 (PAI-1) plays a key role in tissue remodeling and tumor development by suppression of plasminogen activator function. Glucocorticoids (GCs) and transforming growth factor beta (TGF-ß) signal pathways cross-talk to regulate gene expression, but the mechanism is poorly understood. Here we investigated the mechanism and significance of co-regulation of PAI-1 by TGF-ß and dexamethasone (DEX), a synthetic glucocorticoid in ovarian cancer cells. We found that TGF-ß and DEX showed rapidly synergistic induction of PAI-1 expression, which contributed to the early pro-adhesion effects. The synergistic induction effect was accomplished by several signal pathways, including GC receptor (GR) pathway and TGF-ß-activated p38MAPK, ERK and Smad3 pathways. TGF-ß-activated p38MAPK and ERK pathways cross-talked with GR pathway to augment the expression of PAI-1 through enhancing DEX-induced GR phosphorylation at Ser211 in ovarian cancer cells. These findings reveal possible novel mechanisms by which TGF-ß pathways cooperatively cross-talk with GR pathway to regulate gene expression.

The defense potential of glutathione-ascorbate dependent detoxification pathway to sulfur dioxide exposure in Tagetes erecta.

Sulfur dioxide (SO2) exposure is associated with increased risk of various damages to plants. However, little is known about the defense response in ornamental plants. In this study, an artificial fumigation protocol was carried out to study the defense potential of the glutathione (GSH)-ascorbate (AsA) dependent detoxification pathway to SO2 exposure in Tagetes erecta. The results show that when the plants were exposed to different doses of SO2 (0, 15, 30, 50 or 80 mg m(-3)) for different times (6, 12, 18, 24 or 33 h), SO2 induced oxidative stress was confirmed by the increased hydrogen peroxide (H2O2), malondialdehyde (MDA) and relative conductivity of membrane (RC) in a dose-dependent manner for different exposure times. However, the increased levels for H2O2, MDA and RC were not significant vis-a-vis the control when SO2 doses and exposure times were lower than 15 mg m(-3)/33 h, 30 mg m(-3)/24 h or 50 mg m(-3)/12 h (p>0.05). The results could be explained by the increases in the content of reduced form of glutathione (GSH), total glutathione (TGSH), ascorbate (AsA), ratio of GSH/GSSG (oxidized form of glutathione), activities of ascorbate peroxidase (APX), glutathione peroxidase (GPX), glutathione reductase (GR) and glutathione S-transferases (GST). On the other hand, exposure to higher doses of SO2 and longer exposure times, the values of the GSH-AsA dependent antioxidative indices decreased significantly (p<0.01), manifested by increased levels of H2O2. Furthermore, the levels of H2O2, MDA and RC varied little when SO2 doses and exposure times reached a 'critical' value (50 mg m(-3)/24 h). The defense ability of T. erecta to SO2 reached nearly extremity. To summarize, the response of T. erecta to elevated SO2 was related to higher H2O2 levels. GSH-AsA dependent detoxification pathway played an important role in against SO2-induced toxicity, although the defense response could not sufficiently alleviate oxidative damage when SO2 doses and exposure times reached critical value.

Up-regulation of stomatin expression by hypoxia and glucocorticoid stabilizes membrane-associated actin in alveolar epithelial cells.

Stomatin is an important lipid raft-associated protein which interacts with membrane proteins and plays a role in the membrane organization. However, it is unknown whether it is involved in the response to hypoxia and glucocorticoid (GC) in alveolar epithelial cells (AEC). In this study we found that hypoxia and dexamethasone (dex), a synthetic GC not only up-regulated the expression of stomatin alone, but also imposed additive effect on the expression of stomatin in A549 cells, primary AEC and lung of rats. Then we investigated whether hypoxia and dex transcriptionally up-regulated the expression of stomatin by reporter gene assay, and found that dex, but not hypoxia could increase the activity of a stomatin promoter-driven reporter gene. Further deletion and mutational studies demonstrated that a GC response element (GRE) within the promoter region mainly contributed to the induction of stomatin by dex. Moreover, we found that hypoxia exposure did not affect membrane-associated actin, but decreased actin in cytoplasm in A549 cells. Inhibiting stomatin expression by stomatin siRNA significantly decreased dense of peripheral actin ring in hypoxia or dex treated A549 cells. Taken all together, these data indicated that dex and/or hypoxia significantly up-regulated the expression of stomatin in vivo and in vitro, which could stabilize membrane-associated actin in AEC. We suppose that the up-regulation of stomatin by hypoxia and dex may enhance the barrier function of alveolar epithelia and mediate the adaptive role of GC to hypoxia.

Induction of small G protein RhoB by non-genotoxic stress inhibits apoptosis and activates NF-κB.

It has been reported by us and other groups that the expression of small GTP binding protein RhoB can be induced by genotoxic stressors and glucocorticoid (GC), a stress hormone that plays a key role in stress response. Until now stress-induced genes that confer cytoprotection under stressed conditions are largely unknown. In this study, we investigated the effects and mechanism of non-genotoxic stressors, including scalding in vivo and heat stress in vitro on the expression of RhoB. We found for the first time that both scalding, which could induce typical neuroendocrine responses of acute stress and cellular heat stress significantly increased the expression of RhoB at mRNA and protein levels. Moreover, in vitro experiments in human lung epithelial cells (A549) showed that induction of RhoB by heat stress was in a glucocorticoid receptor (GR)-independent manner and through multiple pathways including stabilization of RhoB mRNA and activation of p38 MAPK. Further experiments demonstrated that up-regulation of RhoB significantly inhibited heat stress-induced apoptosis and elevated transcriptional activity of NF-κB, but did not affect the expression of Hsp70 in A549 cells. In conclusion, we showed for the first time that RhoB was up-regulated by scalding in vivo and heat stress in vitro and played an important cytoprotective role during heat stress-induced apoptotic cell death.

Expression of Gli1 correlates with the transition of breast cancer cells to estrogen-independent growth.

The failure of breast cancer treatment is largely due to the development of estrogen independence. Current data illustrate that Hedgehog (Hh) signaling may play an important role in breast cancer development. Here, we show that the expression of the Hh effector protein, Gli1 was significantly higher in estrogen-independent breast cancer cells than in estrogen-dependent cells. Our data showed for the first time that stable expression of Gli1 in ER positive breast cancer cell lines MCF-7 and T47D can induce estrogen-independent proliferation and promote G1/S phase transition, which associated with cyclin-Rb axi. Gli1 can also attenuate the response of proliferation to estrogenic stimulation, which was correlated with down-regulation of expression of ERalpha and PR, as well as down-regulation of transactivation of ERalpha. Our results suggest that up-regulation of Gli1 in breast cancer cells may be one of the mechanisms responsible for developing estrogen independence and this process may be regulated through down-regulation of expression and transactivation of ERalpha.

An MYB transcription factor from Malus xiaojinensis has a potential role in iron nutrition.

Regulation of iron uptake and use is critical for plant survival and growth. We isolated an MYB gene from Malus xiaojinensis named MxMYB1, which is induced under Fe-deficient conditions. Expression of MxMYB1 was upregulated by Fe starvation in the roots but not in leaves, suggesting that MxMYB1 might play a role in iron nutrition in roots. Transgenic Arabidopsis plants expressing MxMYB1 exhibited lower iron content as compared with wild type plants under both Fe-normal (40 microM) and Fe-deficient conditions (Fe omitted and Ferrozine 300 microM). However, the contents of Cu, Zn and Mn were not changed in these transgenic plants. Gene chip and real-time polymerase chain reaction analyses indicated that the expression of two Fe-related genes encoding an iron transporter AtIRT1 and an iron storage protein ferritin AtFER1 might be negatively regulated by MxMYB1 as the expression levels of these genes were lower in MxMYB1 expressing transgenic Arabidopsis plants as compared with wild type plants under both Fe-normal and Fe-deficient conditions. These results suggest that MxMYB1 may function as a negative regulator of iron uptake and storage in plants.