AIM:To investigate the effect of calcitonin gene related peptide(CGRP)on the expression of cyclic AMP response element binding protein(CREB)and phosphorylated-CREB in rat parietal cortex during focal cerebral ischemia/reperfusion(I/R).METHODS:Focal cerebral ischemia/reperfusion model was induced by occlusion of the right middle cerebral artery using the intraluminal suture method.The expressions of CREB and phospho-CREB in the parietal cortex in different groups(sham group,focal cerebral ischemia/reperfusion group and CGRP group)were detected with immunohistochemistry and Western blotting,and the positive products were analyzed by image analysis system.RESULTS:There was definite expression of CREB in right parietal cortex in sham group,while it was lesser in I/R group than that in sham group,but it became more in CGRP group than that in I/R group(P

Aim To explore the effect of exogenous nerve growth factor(NGF) on tau hyperphosphorylation in rat hippocampus during focal cerebral ischemia/reperfusion(I/R).Methods Focal cerebral ischemi-a/reperfusion model was induced by occlusion of the right middle cerebral artery using the intraluminal suture method.The level of tau hyperphosphorylation at Ser199/202 site and total tau in rat ispolateral hippocampal CA1 regions during focal cerebral ischemia/reperfusion were detected by SABC immunohistochemical method and Western blot,and the positive products were analyzed by image analysis system.Results The level of tau hyperphosphorylation at Ser199/202 site and total tau in rat hippocampal CA1 regions were significantly higher in I/R group than that in sham group(P

The mechanisms that specify and maintain the characteristics of germ cells during animal development are poorly understood. In this study, we demonstrated that loss of function of the zinc-finger gene lsy-2 results in various somatic cells adopting germ cells characteristics, including expression of germline-specific P granules, enhanced RNAi activity and transgene silencing. The soma to germ transformation in lsy-2 mutants requires the activities of multiple chromatin remodeling complexes, including the MES-4 complex and the ISW-1 complex. The distinct germline-specific features in somatic cells and the gene expression profile indicate that LSY-2 acts in the Mec complex in this process. Our study demonstrated that lsy-2 functions in the maintenance of the soma-germ distinction.
Adenosine Triphosphatases ; genetics ; metabolism ; Animals ; Animals, Genetically Modified ; Caenorhabditis elegans ; genetics ; metabolism ; Caenorhabditis elegans Proteins ; genetics ; metabolism ; Fluorescent Antibody Technique, Indirect ; Gene Expression Profiling ; Genes, Essential ; genetics ; Germ Cells ; metabolism ; Green Fluorescent Proteins ; genetics ; metabolism ; Mutation ; RNA Interference ; Transcription Factors ; genetics ; metabolism

OBJECTIVETo investigate the effect of betulinic acid (BA) on the proliferation, migration, apoptosis and cell cycle of pancreatic cancer cells (BxPC-3) in vitro and elucidate the underlying.

METHODThe effect of BA on the proliferation of BxPC-3 was measured by using sulforhodamine B (SRB) assay. Migratory ability of BxPC3 cells were detected by wound healing assay, and the morphological change was observed with light microscope. The influence of BA on cell cycle of BxPC-3 cells was tested by flow cytometry (FCM). Apoptosis was analyzed by using Hochest33342-PI double staining. Western blot technologies were applied to detect the expression of Bcl-2 and Bax.

RESULTBA exhibited significant cell proliferation and migration inhibition, as well as its potency of inducing apoptosis in BxPC-3 cells in vitro in a dose-dependent manner. The IC50 value for 72 h was 16.54 mg x L(-1). Cell migration was significantly inhibited at 5 mg x L(-1) of BA. Cells treated with BA showed increased cell population in G0 phase, with decreased G2/M phase population. The expression of Bax and Bcl-2 was up and down-regulated respectively in BA-treated BxPC-3 cells in a dose-dependent manner.

CONCLUSIONBA exerted potent effect on growth inhibition, G0 cell cycle arrest and induction of apoptosis in BxPC-3 cells in vitro, possibly associated with the down-regulation of Bcl-2 and up-regulation of Bax expression. The potent antitumor capacity of BA suggested that it could be a promising new anticancer agent in human pancreatic cancer treatment.

Apoptosis ; drug effects ; Cell Cycle ; drug effects ; Cell Line, Tumor ; Cell Movement ; drug effects ; Cell Proliferation ; drug effects ; Drugs, Chinese Herbal ; pharmacology ; Gene Expression Regulation, Neoplastic ; drug effects ; Humans ; Pancreatic Neoplasms ; drug therapy ; genetics ; metabolism ; physiopathology ; Proto-Oncogene Proteins c-bcl-2 ; genetics ; metabolism ; Triterpenes ; pharmacology ; bcl-2-Associated X Protein ; genetics ; metabolism

Sec61β, a subunit of the Sec61 translocon complex, is not essential in yeast and commonly used as a marker of endoplasmic reticulum (ER). In higher eukaryotes, such as Drosophila, deletion of Sec61β causes lethality, but its physiological role is unclear. Here, we show that Sec61β interacts directly with microtubules. Overexpression of Sec61β containing small epitope tags, but not a RFP tag, induces dramatic bundling of the ER and microtubule. A basic region in the cytosolic domain of Sec61β is critical for microtubule association. Depletion of Sec61β induces ER stress in both mammalian cells and Caenorhabditis elegans, and subsequent restoration of ER homeostasis correlates with the microtubule binding ability of Sec61β. Loss of Sec61β causes increased mobility of translocon complexes and reduced level of membrane-bound ribosomes. These results suggest that Sec61β may stabilize protein translocation by linking translocon complex to microtubule and provide insight into the physiological function of ER-microtubule interaction.
Animals ; COS Cells ; Caenorhabditis elegans Proteins ; genetics ; metabolism ; Cell Line, Tumor ; Cercopithecus aethiops ; Endoplasmic Reticulum ; metabolism ; Homeostasis ; Humans ; Microtubules ; metabolism ; SEC Translocation Channels ; deficiency ; genetics ; metabolism