Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P11021 (BiP)
 2,049 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The post-translational modifications of the G protein of vesicular stomatitis virus, described in the preceding paper, indicate that its transport is arrested by carbonylcyanide m-chlorophenylhydrazone (CCCP) in or near the trans-Golgi. Immunofluorescence microscopy of BHK-21 cells infected with vesicular stomatitis virus and treated with CCCP shows an accumulation of G protein in the Golgi area. In the same cells, the morphology of wheat germ agglutinin (WGA)-staining structures in the perinuclear region is aberrant. Using anti-BiP antibody, there is no obvious change in the structure of the endoplasmic reticulum. Electron microscopy reveals that the aberrant structures in the perinuclear region result from dilation of Golgi cisternae and accumulation of large vacuoles near the Golgi stack. The appearance of these aberrant structures is dose-dependent and they disappear after the protonophore is removed. The vast majority of the vacuoles accumulate on the trans side of the Golgi stack. A small fraction of them contain the marker enzyme thiamine pyrophosphatase (TPPase). By immunoelectron microscopy, most of the vacuoles contain G protein. We conclude that most of the Golgi-associated vacuoles are derived from a distal Golgi transport compartment, possibly the trans-Golgi reticulum, and that CCCP reversibly inhibits the transport of newly synthesized G protein through this distal compartment.
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PMID:The glycoprotein of VSV accumulates in a distal Golgi compartment in the presence of CCCP. 255 60

Human hepatocellular carcinoma (HCC) is one of the commonest causes of mortality among solid organ malignancies. The incidence of HCC in the United States is rising. Few proteomic biomarker studies have been done in U.S. populations. Tumor and nonmalignant tissue from three American patients with hepatitis and non-hepatitis-associated HCC were analyzed to find common differences in protein expression. Proteins were separated by 2D electrophoresis (isoelectric focusing followed by 10% SDS-PAGE). Gels were fixed and then stained with Coomassie brilliant blue. Digitization and processing were performed using the PDQuest software. The Student's t-test was used to detect quantitative protein changes between tumor and nonmalignant liver consistent in all sample pairs with a cutoff made at P < 0.01. This yielded a total of 20 spots with significant (>2 fold) abundance changes. Matrix-assisted laser desorption ionization mass spectrometry analysis was performed using Waters Micomass M@LDI SYSTEM. The proteins were then identified using manual ProFound. Among the 20 spots, 10 showed overexpression and 10 showed underexpression in tumor. Overexpressed proteins included beta-5-tubulin, beta-actin, vimentin, hypermethylated in cancer 2 protein, heat-shock 70-kDa protein 9B, serum albumin, 39S ribosomal protein L45, butyrophilin, autoimmune regulator, and transcription factor ETV7. Underexpressed proteins included BiP protein, superoxide dismutase, peroxiredoxin 2, inoraganic pyrophosphatase, keratin 8, carbonic anhydrase 1, repulsive guidance molecule, catalase, C-1-tetrahydrofolate synthase, and hemoglobin alpha-2. Of particular interest, the protein autoimmune regulator was expressed 14-fold higher in tumor tissue, suggesting it may have a role in HCC. Validation and further investigation of these protein changes may lead to the discovery of new molecular targets for therapy, biomarkers for early detection, and new endpoints for therapeutic efficacy and toxicity.
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PMID:A pilot study of proteomic profiles of human hepatocellular carcinoma in the United States. 1953 95