Meeting Reports

Analysis of Autophagy Regulation: Discussion of recent research and new technologies

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Meeting report from the Euroscicon event: 3rd October 2013, Cineworld: The O2, London, UK

Meeting Chair: Dr. Gary Warnes

Blizard Institute, Barts & The London School of Medicine & Dentistry, Queen Mary University

 Author: Dr Eleftherios Karanasios, Babraham Institute,

Babraham Research Campus, Cambridge

Editors: Dr Astrid Englezou and Dr Shara Cohen

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This one-day meeting “Analysis of Autophagy Regulation: Discussion of recent research and new technologies” organized by Euroscicon, was held on the 3rd of October 2013, in London, UK.  Autophagy is a membrane trafficking pathway that cells activate under diverse stress conditions to deliver cytosolic material for degradation to lysosomes. Different techniques were presented, to study the regulation of autophagy, with special emphasis on imaging and flow cytometric assays. Speakers from diverse disciplines presented data, which included the basic mechanisms of autophagosome formation and the role of autophagy in human physiology and disease, including neurodegeneration, cancer and infectious diseases. The understanding of autophagy and its implications for human health and disease has come a long way in the last few years. Novel technologies were presented, in this meeting, which will aid the understanding of autophagy regulation at the molecular level

aoardorrant

  • Format: Kindle Edition
  • File Size: 956 KB
  • Print Length: 34 pages
  • Publisher: Honnao (January 2, 2014)
  • Sold by: Amazon Digital Services, Inc.
  • Language: English
  • ASIN: B00HNR1M8M

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Contents

Abstract

FLOW CYTOMETRIC MEASUREMENT OF CELL ORGANELLE PHAGY

AUTOPHAGY AND NEURODEGENERATION

A ROLE FOR Rab8 AND AUTOPHAGY IN THE REGULATION OF SYNAPSE GROWTH

AUTOPHAGY AS A BARRIER TO VIRAL AND NON-VIRAL GENE DELIVERY

17-BETA-ESTRADIOL AND PROGESTERONE ENHANCE EXPRESSION OF AUTOPHAGIC GENES IN BOVINE MAMMARY EPITHELIAL CELLS

INDUCTION OF AUTOPHAGY IN CHRONIC MYELOID LEUKAEMIA FOLLOWING TREATMENT WITH TYROSINE KINASE INHIBITORS MAY CONTRIBUTE TO DISEASE PERSISTENCE

THE CORE AUTOPHAGY PROTEIN ATG4B IS CRITICAL TO THE SURVIVAL OF LEUKEMIC STEM/PROGENITOR CELLS AND PREDICTS CLINICAL OUTCOMES OF CML PATIENTS TREATED WITH IMATINIB THERAPY

DYNAMIC ASSOCIATION OF THE ULK1 COMPLEX WITH OMEGASOMES DURING AUTOPHAGY INDUCTION

MOLECULAR MECHANISMS OF MAMMALIAN AUTOPHAGY

AUTOPHAGY IN HOST-PATHOGEN INTERACTION

Executive summary

About the Author

About the Chair

About the Speakers

David Rubinsztein

Agnes Foeglein

Sean T Sweeney

Sharon A. Tooze

Tom Wileman

Abstracts of oral and poster presentations

17BETA-ESTRADIOL AND PROGESTERONE ENHANCE EXPRESSION OF AUTOPHAGIC GENES IN BOVINE MAMMARY EPITHELIAL CELLS.

INDUCTION OF AUTOPHAGY IN CHRONIC MYELOID LEUKAEMIA FOLLOWING TREATMENT WITH TYROSINE KINASE INHIBITORS MAY CONTRIBUTE TO DISEASE PERSISTENCE

THE CORE AUTOPHAGY PROTEIN ATG4B IS CRITICAL TO THE SURVIVAL OF LEUKEMIC STEM/PROGENITOR CELLS AND PREDICTS CLINICAL OUTCOMES OF CML PATIENTS TREATED WITH IMATINIB THERAPY

DYNAMIC ASSOCIATION OF THE ULK1 COMPLEX WITH OMEGASOMES DURING AUTOPHAGY INDUCTION

AGGREGATION OF MISFOLDED PROTEINS AND THEIR CLEARANCE BY AUTOPHAGY; RELEVANCE TO NEUROPSYCHIATRIC DISEASES

17-BETA-ESTRADIOL AND PROGESTERONE REGULATES AUTOPHAGY DURING FUNCTIONAL DEVELOPMENT OF ALVEOLAR STRUCTURES FORMED BY BOVINE MAMMARY EPITHELIAL CELLS CULTURED IN 3D SYSTEM

CLEARANCE OF DYING RETINAL PIGMENT EPITHELIAL (RPE) CELLS BY PROFESSIONAL AND NON-PROFESSIONAL PHAGOCYTES AS IN VITRO MODEL FOR AGE-RELATED MACULAR DEGENERATION (AMD)

STIMULATION OF AUTOPHAGY AS A POTENTIAL TREATMENT FOR CHONDRODYSPLASIA CAUSED BY COLLAGEN X MUTATIONS

CROSS-TALK BETWEEN AUTOPHAGY AND APOPTOSIS IN LONG-TERM CULTURES OF BLOOD NEUTROPHILS

EXAMINATION OF COMMON GENE TARGETS FOR β-CATENIN AND NFkB PROTEINS IN IMATINIB SENSITIVE AND RESISTANT K562 CELL LINES

EFFECT OF NILOTINIB ON INFLAMMATORY MARKERS IN LPS/IFNγ ACTIVATED RAW 264.7 MACROPHAGES

INTERACTION OF NFΚB AND AKIRIN PROTEINS IN IMATINIB RESISTANT AND SENSITIVE K562 CELL LINES.

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