Misfolded growth hormone causes fragmentation of the Golgi apparatus and disrupts endoplasmic reticulum-to-Golgi traffic

Journal of Cell Science

Volumn 114, Issue 20, 2001, Pages 3685-3694

  Graves, T K ^a   Patel, S ^a   Dannies, P S ^a   Hinkle, P M ^a  

^a UNIVERSITY OF ROCHESTER SCHOOL OF MEDICINE AND DENTISTRY   (United States)

Author keywords

Golgi apparatus; Growth hormone; Unfolded protein response

Indexed keywords

ALKALINE PHOSPHATASE; ALPHA TUBULIN; BIOLOGICAL MARKER; GROWTH HORMONE; MEMBRANE PROTEIN; MEMBRIN; MESSENGER RNA; PROLACTIN; PROTIRELIN RECEPTOR; SECRETORY PROTEIN; UNCLASSIFIED DRUG;

AMINO ACID SEQUENCE; ANIMAL CELL; ARTICLE; CELL MEMBRANE; CELL TRANSPORT; CONTROLLED STUDY; CYTOPLASM; CYTOTOXICITY; ENDOPLASMIC RETICULUM; GENE DELETION; GENETIC TRANSFECTION; GOLGI COMPLEX; GROWTH HORMONE DEFICIENCY; HOST CELL; HUMAN; IMMUNOHISTOCHEMISTRY; IMMUNOREACTIVITY; MICROTUBULE ASSEMBLY; NONHUMAN; PHARMACOLOGY; PREVENTION; PRIORITY JOURNAL; PROTEIN EXPRESSION; PROTEIN FOLDING; PROTEIN LOCALIZATION; RECEPTOR BINDING; STAINING; THERAPY;

ALKALINE PHOSPHATASE; ANIMALS; ANTI-BACTERIAL AGENTS; BIOLOGICAL MARKERS; CARRIER PROTEINS; CHROMATIN; COATOMER PROTEIN; COS CELLS; ENDOPLASMIC RETICULUM; GOLGI APPARATUS; GREEN FLUORESCENT PROTEINS; HEAT-SHOCK PROTEINS; HUMAN GROWTH HORMONE; HUMANS; INDICATORS AND REAGENTS; LUMINESCENT PROTEINS; MEMBRANE PROTEINS; MICROTUBULE-ORGANIZING CENTER; MICROTUBULES; MOLECULAR CHAPERONES; PROLACTIN; PROTEIN FOLDING; PROTEIN TRANSPORT; QB-SNARE PROTEINS; RECEPTORS, THYROTROPIN-RELEASING HORMONE; TUNICAMYCIN;

ANIMALIA;

EID: 0034764940     PISSN: 00219533     EISSN: None     Source Type: Journal    
DOI: None     Document Type: Article

References (44)

1. Cargo can modulate COPII vesicle formation from the endoplasmic reticulum
2. Visualization of the thyrotropin-releasing hormone receptor and its ligand during endocytosis and recycling
3. Secreted placental alkaline phosphatase: A powerful new quantitative indicator of gene expression in eukaryotic cells
4. Dynamic interaction of BiP and ER stress transducers in the unfolded-protein response
5. Intracellular signaling from the endoplasmic reticulum to the nucleus
6. Familial growth hormone deficiency: A model of dominant and recessive mutations affecting a monomeric protein
7. A recurring dominant negative mutation causes autosomal dominant growth hormone deficiency - A clinical research center study
8. Golgi dispersal during microtubule disruption: Regeneration of Golgi stacks at peripheral endoplasmic reticulum exit sites
9. BiP expression is not increased by the accumulation of PiZ alpha 1-antitrypsin in the endoplasmic reticulum
10. Human growth hormone and extracellular domain of its receptor: Crystal structure of the complex
11. Setting the standards: Quality control in the secretory pathway
12. Molecular cloning, characterization, and dynamics of rat formiminotransferase cyclodeaminase, a Golgi-associated 58-kDa protein
13. Accumulation of the insoluble PiZ variant of human alpha 1-antitrypsin within the hepatic endoplasmic reticulum does not elevate the steady-state level of grp78/BiP
14. Site-directed mutagenesis by overlap extension using the polymerase chain reaction
15. Immunoisolation and characterization of a subdomain of the endoplasmic reticulum that concentrates proteins involved in COPII vesicle biogenesis
16. Molecular basis of autosomal dominant neurohypophyseal diabetes insipidus. Cellular toxicity caused by the accumulation of mutant vasopressin precursors within the endoplasmic reticulum
17. Aggresomes: A cellular response to misfolded proteins
18. Structure and function in rhodopsin. 7. Point mutations associated with autosomal dominant retinitis pigmentosa
19. Endocrinopathies in the family of endoplasmic reticulum (ER) storage diseases: Disorders of protein trafficking and the role of ER molecular chaperones
20. Ultrastructural analysis of apoptosis induced by the monoclonal antibody anti-APO-1 on a lymphoblastoid B cell line
21. Folding of secretory and membrane proteins
22. Autosomal dominant growth hormone (GH) deficiency type II: The Del32-71-GH deletion mutant suppresses secretion of wild-type GH
23. A SNARE involved in protein transport through the Golgi apparatus
24. 2+ based on green fluorescent proteins and calmodulin
25. Glycoproteins form mixed disulphides with oxidoreductases during folding in living cells
26. Tripartite management of unfolded proteins in the endoplasmic reticulum
27. Beta-COP localizes mainly to the cis-Golgi side in exocrine pancreas
28. Misfolded proteins in the endoplasmic reticulum
29. Genetic basis of endocrine disease. 6. Molecular basis of familial human growth hormone deficiency
30. Vaccinia virus infection disrupts microtubule organization and centrosome function
31. Misfolded major histocompatibility complex class I molecules accumulate in an expanded ER-Golgi intermediate compartment
32. Blockade of membrane transport and disassembly of the Golgi complex by expression of syntaxin 1A in neurosecretion-incompetent cells: Prevention by rbSEC1
33. Structural elements common to mitosis and apoptosis
34. Inhibition of phosphatidic acid synthesis alters the structure of the Golgi apparatus and inhibits secretion in endocrine cells
35. The unfolded protein response: An intracellular signalling pathway with many surprising features
36. Rhodopsin mutations responsible for autosomal dominant retinitis pigmentosa. Clustering of functional classes along the polypeptide chain
37. Aphidicolin induces alterations in Golgi complex and disorganization of microtubules of HeLa cells upon long-term administration
38. Molecular pathogenesis of liver disease in alpha1-antitrypsin deficiency
39. Role of microtubules in the organization of the Golgi complex
40. Functional and genomic analyses reveal an essential coordination between the unfolded protein response and ER-associated degradation
41. A mutation in the insulin 2 gene induces diabetes with severe pancreatic beta-cell dysfunction in the Mody mouse
42. Cytochemical and ultrastructural examination of apoptotic odontoclasts induced by bisphosphonate administration
43. A lag in intracellular degradation of mutant alpha 1-antitrypsin correlates with the liver disease phenotype in homozygous PiZZ alpha 1-antitrypsin deficiency
44. Signal transduction, desensitization, and recovery of responses to thyrotropin-releasing hormone after inhibition of receptor internalization