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Registration open: EMBO Workshop Autophagy, August 26th - 30th, 2017, Crieff, Scotland, United Kingdom

April 2019
"Autophagy: From molecular principles to human diseases" is the topic of this year's EMBO Workshop on Autophagy. Register here until April 26.



3Cs technology opens new horizons for production of highly complex CRISPR/Cas libraries.

6th March 2019
As published today in eLife, a team around IBC2 Group Leader Manuel Kaulich has developed a new technology for generating CRISPR/Cas gene perturbation reagents. They dubbed their innovation as "3Cs", as gRNA are synthesized as covalently-closed circles. It enables the fast and, most importantly, cloning-free production of gRNA and shRNA libraries. By this, the 3Cs technology overcomes one of the major caveats of conventional library production. Another advantage is that the 3Cs technology uncouples sequence diversity from sequence distribution, thereby removing an often-observed bias in the production process and rendering high quality reagents in any order of magnitude. Groundbreaking discoveries can hardly ever be planned, and this one came over a coffee break. Manuel and Andreas Ernst, who at that time also headed an IBC2 group, were talking about their different areas of expertise, and suddenly the idea emerged on how to elegantly combine strategies used in phage display with gene editing. With support of Innovectis GmbH, Goethe University's Tech Transfer Office, they immediately applied for patent protection. To prove performance of 3Cs gene editing reagents in cells, together with the group of IBC2 Group Leader Anja Bremm a library targeting all human deubiquitinating enzymes (DUBs) was produced and their function for cell fitness identified. Then, the team around Manuel went on to generate the largest gRNA library known to date. This so-called oTGW (optimized truly genome wide) library targets 16.5 million unique sites throughout the human genome, both in coding and non-coding regions. The oTGW library has a great potential to fuel future functional genomics studies and is available for the scientific community via the Goethe University Depository. Together with IBC2 Director Ivan Dikic, Manuel set up the Frankfurt CRISPR/Cas Screening Center (FCSC).

Link to GU press release in English
Link to original article
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Christian Münch appointed as member of the Johanna Quandt Young Academy at Goethe (JQYA).

23rd January 2019
IBC2 group leader Christian Münch was recently admitted as a member to the JQ Young Academy. Within the "Science funding" program of JQYA, Christian will now receive financial support for his independent research group until October 2023. The Münch group is deciphering quality responses upon mitochondrial protein misfolding, a field with very high biomedical impact. Misfolding of mitochondrial proteins occurs e.g. as part of neurodegeneration, and little is known about how cellular response mechanisms contribute to the onset of respective diseases and their progression. The JQYA is an independent academy within Goethe University which foster researchers at the start of their independent careers.

Link to Johanna Quandt Young Academy at Goethe (JQYA)
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List of Highly Cited Researchers released.

27th November 2018
IBC2 Director Ivan Dikic is one of the worlds' most influential scientists as revealed by Clarivate Analytics' Highly Cited Researchers List. He has been selected for his exceptional performance in the newly introduced category "Cross-Field", based on his multiple high impact papers published across several fields. The methodology used by Clarivate Analytics to curate this annual list aims at identifying scientists who have substantial contemporary impact. It is calculated from the number of highly cited papers produced, with a highly cited paper being defined as ranking amongst the top 1% as measured by citations for the field and year. Approximately 6,000 researchers worldwide are named in this years' list. The papers analyzed were published between 2006 to 2016. Besides Ivan Dikic, 12 other colleagues from Goethe University have been credited by the 2018 list. With this result, Goethe University is second best in Germany, only Heidelberg University scores higher. The global pole position is traditionally taken by Harvard University.

Link to the list
Link to Clarivate's press release
Link to Press Release by Goethe University
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Ivan Dikic is appointed as Max Planck Fellow.

October 2018
As announced by the Max Planck Institute (MPI) of Biophysics today, IBC2 Director Ivan Dikic has been appointed as Fellow of the Max Planck Society and will start his 5-year-term immediately, including supervision of a small working group at the Frankfurt-based Institute. The Max Planck Fellow Programme has been set up to strengthen cooperation between outstanding university professors and Max Planck Society researchers. Research in the Dikic group is centered around two major cellular quality control pathways: the ubiquitin system and autophagy. As such they provide protection against various human diseases and are involved in almost all cellular signaling processes. The group covers a wide range of expertise to reveal structure-function relationships. Recently, the Dikic group revealed a novel ubiquitination mechanism induced by bacterial enzymes upon infection of human cells. In collaboration with colleagues at the MPI of Biophysics, the group now aims to resolve additional atomic details of this serine ubiquitination. A second area of mutual interest is in remodeling of endoplasmic reticulum via a process known as ER-phagy. Until now, very little is known about the mechanisms facilitating membrane targeting, bending and shaping during this selective form of autophagy. In addition, Ivan aims to also build strong links between colleagues at the MPI of Biophysics and the highly competitive cancer research programme at Goethe University. He is one of the founders of the Frankfurt Cancer Institute (FCI), which has recently received significant funding for building up a LOEWE center and a new research building.

Link to MPI of Biophysics
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ERC Starting Grant for Christian Münch.

27th Jul 2018
The European Research Council (ERC) awarded one of its prestigious Starting Grants to Emmy Noether group leader Christian Münch. The grant provides € 1.44 Mio to carry out a challenging project dubbed ‘mitoUPR’, in which Christian plans to unravel the impact of the mitochondrial unfolded protein response (UPRmt) on the cellular environment in mammalian cells. The UPRmt is a poorly understood mitochondrial stress response that activates upon protein misfolding in mitochondria. Münch’s interest in protein quality control processes dates back to his PhD at University of Cambridge (UK), when he was the first to describe the prion-like behavior of mutant SOD1 in ALS. During his postdoctoral tenure at Harvard University (Boston, USA), he discovered a new branch of the UPRmt controlling mitochondrial translation. Within his ERC project, Christian now plans to analyze how the UPRmt influences processes outside the mitochondrion. According to his central hypothesis, the regulation of cellular stress responses is centrally integrated, and he plans to unravel the role of UPRmt within those signaling networks. A second focus is on mitochondrial RNA granules, which are commonly associated with the organelle’s protein production machinery. Despite the fact that mutations in components of those granules are commonly associated with disease, so far little is known about their architecture and especially their regulation upon stress. To achieve his challenging aims, Christian relies on a range of technologies established at IBC2 and aims at developing an in vivo model for studying the UPRmt.

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Christian Münch joins SFB 1177 as project leader

11th Jul 2018
Recently, the German Research Foundation (DFG) has approved Christian Münch’s supplementary proposal to study Mitophagy induction by the mitochondrial unfolded protein response within the framework of SFB 1177. Protein misfolding in mitochondria has been associated with numerous diseases, including neurodegeneration and cancer, and leads to activation of a mitochondrial stress response – the mitochondrial unfolded protein response (UPRmt). For the next two years, Christian Münch will address the role of mitophagy induction by the UPRmt to resolve mitochondrial protein folding defects.

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Stefan Knapp elected as EMBO member

14th May 2018
The European Molecular Biology Organization (EMBO) announces the list of 62 scientists who were elected as members in 2018. Amongst them is Prof. Stefan Knapp, project leader within SFB 1177, therewith joining "a group of more than 1800 of the best researchers in Europe and around the world“, as EMBO states.

EMBO press release Link
EMBO profile of Stefan Knapp Link

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Autophagosomal content profiling reveals novel mitophagy pathway

16th Nov 2017
Until now, little was known about the identity of proteins which are disposed via autophagy. In an unbiased approach to shed light on this conundrum, the Behrends group used a novel proteomics technology to selectively capture all cargo proteins carried by autophagosomes in living cells. The outcome was a long list of 1,147 proteins – amongst them numerous involved in mitochondrial function, a rather unexpected result considering that no treatment triggering mitophagy was applied. The researchers followed up on this and made a yet more surprising discovery: They found that proteins from several mitochondrial subcompartments are directed towards autophagosomes in a piecemeal fashion, meaning without degradation of the entire organelle. This establishes a novel mechanism of mitophagy, which may function to maintain the mitochondrial household under basal growth condition. The study was largely funded by the CRC 1177 ( and carried out at IBC2 and at Ludwig-Maximilians-Universität (LMU) München, to where the Behrends lab recently moved. The results are published in today’s issue of Molecular Cell.

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RTN3 identified as novel ER-phagy receptor.

15th Jun 2017
The endoplasmic reticulum (ER) is the cell’s largest and probably most versatile organelle. It consists of extended membrane structures, which are constantly remodeled to ensure functionality in all cellular states. Degradation of the ER is mediated by a specialized form of selective autophagy (ER-phagy), a process which is until now not very well understood. An international team around Ivan Dikic has identified Reticulon 3 (the full-length form of RTN3) as a selective receptor which specifically triggers fragmentation of ER tubules and their delivery to lysosomes. The process requires the core autophagy machinery but is independent of FAM134B, the first ER-phagy receptor previously identified by Dikic’s group. FAM134B is responsible for targeting ER sheets rather than ER tubules. The scientists were surprised to discover that the full length RTN3 contains six of the so called LIR motifs that are essential for the function of autophagy receptor. Normally, a single LIR motif is sufficient. Most likely, the high amount of LIR motifs leads to a positive amplification loop. The experiments also enabled a broader view on different roles of the RTN protein family, highlighting the importance of discriminating between isoforms which display highly specialized and unique functions. The results have now been published online in eLife (Grumati et al, 2017).

Link to Original article

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15th May 2017
This was the slogan of a public TEDx event in Zagreb, at which IBC2 director Ivan Dikic shared his thoughts about what can be learnt from bacteria. It was the largest Croatian TED event ever, full of enthusiasm, creativity and inspiration. The 20 speakers came from many different areas of society, and all gave one major motivation message: boundaries can be broken if we just strive hard enough. „It was an amazing event, positive and vibrant. The moment when you step out on stage is almost electrifying“, described Ivan Dikic his appearance in the Lisinski Concert Hall which was filled with an audience of 1000. TED is a non-profit organization devoted to spreading great ideas around the globe, TEDx events are independently organized, but follow the same mission of helping communities to spark conversation and connection

Link to picture gallery.
Link to TEDxZagreb.
Link to TED.
Link to the video on Youtube
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Linear ubiquitination controls Salmonella growth

8th May 2017
A team around Ivan Dikic and Mike Heilemann (Chemistry Department, Goethe University) gained unprecedented insight into the mechanism by which cells fight Salmonella infections. Upon intracellular invasion, bacteria are usually rapidly surrounded by a coat of ubiquitin, the function of which remained unclear until now. Combining super-resolution microscopy with cell biological analysis, the researchers now discovered that distinct ubiquitin chains transform the bacterial surface into a molecular signalling platform. They were able to visualize the nanoscale distribution of different ubiquitin chains on the bacterial surface. One chain type, so called linear chains, specifically triggers pro-inflammatory signalling cascades, thereby restricting bacterial proliferation. In addition, the researchers identified the deubiquitinase OTULIN as a regulator capable of limiting this reaction – a very important notion considering the fact that excessive inflammation is one of the major causes of tissue damage following bacterial infection. In collaboration with colleagues from Japan, the Frankfurt researchers now published their results in the latest online issue of Nature Microbiology. Their work is an excellent example for interdisciplinary collaboration and was enabled by funding of several large research networks, e.g. the Cluster of Excellence Macromolecular Complexes, the CRC 1177 on selective autophagy and the LOEWE ubiquitin network. The discovery paves the way for many new projects. Very recently, Ivan Dikic obtained one of the prestigious ERC Advanced Grants in which he will investigate the role of ubiquitin in modulating the host-pathogen interaction in more detail.
Link to publication.
Link to German press release.
Link to English press release.

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How Salmonella tricks the immune system.

13th Jan 2017
Infections with bacterial pathogens represent a global burden and are a major cause of death worldwide. For the design of new treatment paradigms it is essential to understand the intricate interplay between bacterial virulence strategies and host defense. The Dikic laboratory now added the next piece to the puzzle: They elucidated how the Salmonella effector enzyme SopA, a HECT-like E3 ligase, targets two host proteins involved in activating the immune defense (TRIM56 and TRIM65) and triggers their degradation. Atomic details of this new mechanism have now been published in Nature Communications and give a detailed insight into how Salmonella increases its own infectivity by interfering with the host immune response.

Link to publication
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Registration still open: 30th ENCP Congress, September 2nd - 5th, 2017, Paris, France

Symposium on Neuronal Autophagy
SFB 1177 vice speaker Christian Behl will be chairing the symposium „Neuronal autophagy: Concepts and treatment options“ at the 30th ENCP Congress (September 2nd - 5th, 2017, Paris, France).
Registration details and more information
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Fluorescence-based sensors for specifically monitoring autophagy

6th February 2017
Autophagy is a cellular recycling and quality control pathway that is essential for maintaining cellular metabolism and homeostasis. Its malfunction contributes e.g. to neurodegenerative diseases and cancer.
Ubiquitin-like ATG8 proteins constitute central components of the autophagic machinery. However, until today, it is not completely clear why yeast harbors only one ATG8 protein while human cells contain six mammalian ATG8 orthologs, classified into the LC3 and GABARAP subfamilies. Using an interdisciplinary approach combining phage display with additional functional biochemical assays as well as cellular biology, the laboratories of Ivan Dikic and Andreas Ernst now engineered a valuable tool for studying specific functions of LC3 and GABARAP proteins. They developed fluorescence-based sensors that are able to discriminate between the six different members of the mammalian ATG8 protein family and track their actions within cells. As first application, the scientists successfully monitored the involvement of LC3C in selective autophagy of mitochondria (mitophagy) and Salmonella (xenophagy). The joint effort of the Dikic and Ernst groups has been published recently in EMBO Journal and will be helpful in decoding biological functions of individual LC3/GABARAP proteins.
Link to publication.
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Autophagy captures the Nobel Prize.

10th Dec 2016
This year’s Nobel Essay in Cell has been written by Ivan Dikic (IBC2) together with Sharon Tooze (Francis Crick Institute, London). Published on time for the Nobel Ceremony on 10th December, the article highlights milestones leading to the discovery of the molecular principles underlying autophagy by Yoshinori Ohsumi, who is this years’ winner of the Nobel Prize for Medicine or Physiology. Dikic and Tooze tell the story of a simple yet insightful yeast genetic screen that revealed what later was recognized to be one of the most powerful quality-control pathways in cells.

Link to essay in Cell.
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New ubiquitin chemistry regulates life processes

1st December 2016
In the latest issue of Cell, a team around IBC2 director and SFB 1177 speaker Ivan Dikic reveals molecular details of a novel ubiquitination mechanism that may affect numerous life processes. Earlier this year, U.S. colleagues reported that Legionella enzyme SdeA is capable of catalysing ubiquitination single-handedly. Now, the Frankfurt scientists together with collaborators from the MPI for Biology of Ageing (Cologne) have elucidated the chemistry behind and discovered a hitherto unknown type of linkage between ubiquitin and target proteins. Unlike the conventional ubiquitination reaction, the novel one is NAD-dependent, involving an ADP-ribose intermediate and resulting in the attachment of ubiquitin to substrate serine residues via a phosphodiester bond.
While those findings alone are breaking new ground, the discovery went even further: The team showed that the Legionella enzyme does not only transfer ubiquitin onto target proteins, but also leaves behind a complete pool of chemically modified, phosphoribosylated ubiquitin. Phosphoribosylated ubiquitin almost completely inhibits the conventional ubiquitination system and thereby affects essential cellular processes, e.g. proteasomal protein degradation, mitophagy and pro-inflammatory signalling. This explains the pathogenic effects of Legionella infection in immunocompromised patients, who often suffer from extensive lung tissue damage despite antibiotic treatment. The insight generated by the Dikic team may now open the road to the development of new antibacterial agents, which could complement conventional antibiotics by limiting the cellular damage induced by bacterial enzymes.
Link to Cell paper.
Link to German press release.
Link to English press release.
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International marketing concept of UBAUT networks receives DFG award

1st December 2016
As the German Research Foundation (DFG) announced today, Goethe University (GU) is one of the winners of the 2016 Competition for International Research Marketing Ideas. The awarded concept “Let’s talk about UBAUT” was initiated by SFB 1177 on Autophagy (, LOEWE Ub-Net (LINK TO and IBC2, and in collaboration with GU’s Departments for Internationalization and Marketing and Communication. The prize is awarded with 100,000 €, enabling the ubiquitin and autophagy networks now to implement a wide range of marketing measures for increasing their international visibility and attract highly qualified international colleagues to the Rhine Main biomedical research area. The program follows a ‘bottom-up’ approach which will be driven by LOEWE Ub-Net and SFB 1177 scientists. It comprises ambassador visits to renowned research institutions in the US as well as short stipends for international scientists wishing to pursue a career in Germany and a strategy outreach meeting.
Link to DFG press release.
Link to GU press release.
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Nobel Prize in Physiology or Medicine 2016 for autophagy researcher: Congratulations to Yoshinori Ohsumi

3rd October 2016
The Nobel Assembly at Karolinska Institutet decided today that the 2016 Prize is awarded to Yoshinori Ohsumi for his discoveries of mechanisms for autophagy. The Japanese scientist is considered as the founding father of autophagy research: He identified the first autophagy genes in yeast, elucidated the underlying mechanisms and showed that a similar sophisticated machinery exists in human cells. Ohsumi holds a professorship at the Tokyo Institute of Technology in Japan. He is the only Laureate receiving the prize this year, underlining the significance and breakthrough character of his discoveries. The announcement came as fantastic news for the entire field of autophagy research, and the SFB 1177 consortium sends sincerest congratulations to Yoshinori Ohsumi.
Link to the Nobel Academy Press Release
Link to ZDF heute journal report including statement from SFB 1177 member Simone Fulda


SFB 1177 practical course on autophagy

August 2016
The practical course on autophagy, organized by SFB 1177 group leaders Christian Behrends and Christian Pohl, conveyed hands-on experience in autophagy research. In five days, the participants employed biochemical and cell biological assays to study the autophagy pathway and expanded their knowledge on model organisms such as C. elegans as well as on technologies like mass spectrometry and gene editing with CRISPR/Cas9. Daily lectures by senior scientists and group leaders complemented the practical focus of the workshop. By presenting their own preliminary data, both PhD students and Postdocs gained valuable insights into the currently running projects within SFB 1177, sowing the seeds for new collaborations amongst the members of the SFB graduate school. Thanks to all participants for creating a highly supportive and interactive atmosphere fostering the exchange of many experiences and advices!
More info


Frankfurt Conference on Ubiquitin and Autophagy – thanks to all speakers and participants

8th July 2016
From July 4th to 7th, 2016, leading experts in Ubiquitin and Autophagy research from around the world were brought together at Goethe University’s Medical Campus for the first Frankfurt Conference on Ubiquitin and Autophagy, jointly organized by the Cluster of Excellence Macromolecular Complexes, the DKTK site Frankfurt/Mainz, the LOEWE program Ub-Net and SFB 1177. Since the ubiquitin system and autophagy are essential for maintaining cellular integrity and homeostasis, and defects in the two quality control systems are involved in the pathogenesis of numerous diseases, the meeting put emphasis on gaining a more global view on cellular quality control mechanisms, their interconnectivities as well as on exploiting the potential for therapeutic interventions. More than 300 scientists from 12 countries attended the meeting and almost 50 talks in five interdisciplinary sessions covered a broad range of topics from the discovery of basic molecular mechanisms to translation into clinical applications. Moreover, the contribution by early career researchers in vivid discussions and more than 110 poster presentations was overwhelming, as was the quality of the work presented. Coffee breaks, welcome reception and a farewell barbecue at Goethe University’s Westend Campus with a view on the impressive Frankfurt skyline fostered the exchange and interaction amongst the participants giving rise to new ideas, collaborations and insights. The organizers would like to thank all speakers and participants for their active and valuable contribution to the meeting and look forward to the next Frankfurt Conference in 2018.

Interested in Alzheimer’s - register here: "Beyond Amyloid - Widening the View on Alzheimer's Disease“

Herrenhausen Symposium, October 10 & 11 in Hanover, Germany.
Hosted as a Herrenhausen Symposium by the Volkswagen Foundation the meeting aims at bringing together current knowledge on molecular and cellular processes that contribute to AD pathogenesis beyond the so far dominating amyloid hypothesis and at fostering discussion on future perspectives in AD research. Topics to be covered include inflammation, vascular dysfunction, mitochondrial integrity, cell cycle events, lipid metabolism, tau biochemistry, protein misfolding and autophagy. There are no fees to attend the symposium but registration is required.
More info
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Adolf Messer-Stiftungspreis for Anja Bremm.

30th June 2016
Dr. Anja Bremm, group leader of the Molecular Cell Biology Group at IBC2 and Buchmann Institute for Life Sciences (BMLS) was awarded the 2016 Adolf Messer-Stiftungspreis for her research on the physiological role of deubiquitinases (DUBs) in autophagy, endowed by the Adolf Messer Foundation. Stefan Müller, professor of IBC2, held the laudatory speech at the official award ceremony on June 30th, 2016. The prize is conferred annually to early career scientists with an outstanding proven track record to promote pioneering fundamental research projects in natural sciences and medicine and is remunerated with 25.000 €.

Link to Anja Bremm’s research group
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Boehringer Ingelheim Foundation awards Christian Behrends.

14th Apr 2016
Dr. Christian Behrends, group leader of the Autophagy Signaling Group at the IBC2 and part of the SFB 1177 on Selective Autophagy has been selected to be a PLUS3 fellow of the Boehringer Ingelheim Foundation. The foundation will fund his research with a generous support of around 900.000 € for the next three years.

Link to Christian Behrends Lab
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Shedding light on ALS: Novel mechanism in selective autophagy discovered.

29th Mar 2016
ALS (Amyotrophic lateral sclerosis) is a rare and severe disease characterized by loss of motor neurons and neurodegeneration leading to death within 3-4 years. The 2014 ice bucket challenge brought ALS to broader public attention but to date there is no treatment for ALS, despite intensive research in the field. After being involved in the discovery of a kinase (Tank-binding kinase 1, TBK1) linked to ALS (Freischmidt el al., nature neuroscience 2015), researchers from the IBC2 in collaboration with international partners now succeeded in clarifying the physiological function of TBK1. The group around Ivan Dikic revealed that TBK1 specifically phosphorylates its adaptor protein optineurin, thereby enabling a stronger binding of optineurin to ubiquitin that marks damaged mitochondria. By this means, TBK1 promotes an important cellular quality control system responsible for the clearance of damaged mitochondria and other cellular organelles, a process called selective autophagy. Damaged mitochondria, TBK1 and optineurin have long been linked to neurodegenerative diseases such as Parkinson’s and ALS. However, the molecular details behind this connection are only beginning to be unveiled. Benjamin Richter, first author of the study, and his colleagues could further show that an ALS-associated TBK1 mutant fails to associate with optineurin and damaged mitochondria representing a possible link to the disease mechanism underlying ALS. The results are published in this weeks’ PNAS Online Early Edition.

Link to full text article
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Registration open now – Frankfurt Conference on Ubiquitin and Autophagy, July 4-7, 2016

January 2016
Together with the Cluster of Excellence Macromolecular Complexes, the SFB 1177, and the DKTK Frankfurt, LOEWE Ub-Net is organizing the first Frankfurt Conference on Ubiquitin and Autophagy in July 2016. Both the ubiquitin system and autophagy are essential for maintaining cellular integrity and homeostasis. Defects in the two quality control systems are involved in the pathogenesis of numerous diseases. The conference brings together leading experts in this field. Further information and registration here.
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DFG funds autophagy research network

20th Nov 2015
Scientists from Frankfurt and Mainz have successfully applied for funding to establish a Collaborative Research Centre (CRC)/Sonderforschungsbereich (SFB) on the molecular mechanisms of selective autophagy. Autophagy literally means „self-eating“ and describes a process by which the cell recycles harmful ballast like aggregated proteins, damaged organelles or even bacterial invaders. For the next four years, the centre is funded by the German Research Foundation (DFG) with 11 M €. The initiative is led by Ivan Dikic, and is the first large-scale collaborative network in Germany in this highly competitive field.
In the newly established CRC, researchers from the Goethe University, the University Medical Centre in Mainz, the Georg-Speyer-Haus in Frankfurt and the Institute of Molecular Biology in Mainz have teamed up to characterize selective autophagy on the molecular and functional level. This will eventually lead to a better understanding of the role of autophagy in pathophysiology and pave the road for innovative, targeted therapies.
The funding by the DFG will now give a powerful impetus for the network, also strengthening the position of the Rhine Main scientists on the international stage.
Link to German press release.





Chaikuad A, Koschade SE, Stolz A, Zivkovic K, Pohl C, Shaid S, Ren H, Lambert LJ, Cosford NDP, Brandts CH & Knapp S. 2019. Conservation of structure, function and inhibitor binding in UNC-51-like kinase 1 and 2 (ULK1/2). Biochem J, 476, 875-887.


Chakraborty D, Felzen V, Hiebel C, Stuerner E, Perumal N, Manicam C, Grus F, Wolfrum U, Behl C. 2019. Enhanced autophagic-lysosomal activity and increased BAG3-mediated selective macroautophagy as adaptive response of neuronal cells to chronic oxidative stress. Redox Biol, accepted


Christ MG, Huesmann H, Nagel H, Kern A & Behl C. 2019. Sigma-1 receptor activation induces autophagy and increases proteostasis capacity in vitro and in vivo. Cells, 8, pii: E211


Forrester A, De Leonibus C, Grumati P, Fasana E, Piemontese M, Staiano L, Fregno I, Raimondi A, Marazza A, Bruno G, Iavazzo M, Intartaglia D, Seczynska M, van Anken E, Conte I, De Matteis MA, Dikic I, Molinari M, Settembre C. 2019. A selective ER-phagy exerts procollagen quality control via a Calnexin- FAM134B complex. EMBO J, 38, pii:299847


Fottner M, Brunner AD, Bittl V, Horn-Ghetko, Jussupow A, Kaila VRI, Bremm A & Lang K. 2019. Sitespecific ubiquitylation and SUMOylation


Huber J, Obata M, Gruber J, Akutsu M, Löhr F, Rogova N, Guentert P, Dikic I, Kirkin V, Komatsu M, Dötsch V, Rogov VV. 2019. An atypical LIR motif within UFM1-activating enzyme 5 (UBA5) reveals an alternative function for GABARAP proteins. Autophagy, accepted.


Juretschke T, Beli P & Dikic I. 2019. Quantitative phosphoproteomics of selective autophagy receptors. pages 691–701, In: Autophagy; Methods in Molecular Biology. Vol. 1880 (eds. Ktistakis N and Florey O). Humana Press, New York.


Key J, Mueller AK, Gispert S, Matschke L, Wittig I, Corti O, Muench C, Decher N, Auburger G. 2019. Ubiquitylome profiling of Parkin-null brain reveals dysregulation of calcium homeostasis factors ATP1A2, Hippocalcin and GNA11, reflected by altered firing of noradrenergic neurons. Neurobiol Dis, 127, 114- 130.


Lim R, Sugino T, Nolte H, Andrade J, Zimmermann B, Shi C, Doddaballapur A, Ong YT, Wilhelm K, Fasse JWD, Ernst A, Kaulich M, Husnjak K, Boettger T, Guenther S, Braun T, Krueger M, Benedito R, Dikic I. Potente M. 2019. Deubiquitinase USP10 regulates Notch signaling in the endothelium. Science, 364, 188-193.


Nguyen TD, Shaid S, Vakhrusheva O, Koschade SE, Klann K, Thölken M, Baker F, Zhang J, Oellerich T, Sürün D, Derlet A, Haberbosch I, Eimer S, Osiewacz HD, Behrends C, Münch C, Dikic I, Brandts CH. 2019. Loss of the selective autophagy receptor p62 impairs murine myeloid leukemia progression and mitophagy. Blood, 133, 168-179.


Poluzzi C, Nastase MV, Zeng-Brouwers J, Roedig H, Hsieh LTH, Michaelis JB, Buhl EM, Rezende F, Manavski Y, Bleich A, Boor P, Brandes RP, Pfeilschifter J, Stelzer EHK, Muench C, Dikic I, Brandts C, Iozzo RV, Wygrecka M & Schaefer L. 2019. Biglycan evokes autophagy in macrophages via a novel CD44/Toll-like receptor 4 signaling axis: Impact on renal ischemia/reperfusion injury. Kidney Int, 95, 540- 562


Roedig H, Nastase MV, Wygrecka M & Schaefer L. 2019. Breaking down chronic inflammatory diseases: the role of biglycan in promoting a switch between inflammation and autophagy. FEBS J, doi: 10.1111/febs.14791


Van Well EM, Bader V, Patra M, Sánchez-Vicente A, Meschede J, Furthmann N, Schnack C, Blusch A, Longworth J, Petrasch-Parwez E, Mori K, Arzberger, Trümbach D, Angersbach L, Showkat C, Sehr DA, Berlemann LA, Goldmann P, Clement AM, Behl C, Woerner AC, Saft C, Wurst W, Haass C, Ellrichmann G, Gold R, Dittmar G, Hipp MS, Hartl FU, Tatzelt J, Winklhofer KF. 2019. A protein quality control pathway regulated by linear ubiquitination. EMBO J, pii: e100730.


Wegner M, Diehl V, Bittl V, de Bruyn R, Wiechmann S, Matthess Y, Hebel M, Hayes MG, Schaubeck S, Benner C, Heinz S, Bremm A, Dikic I, Ernst A, Kaulich M. 2019. Circular synthesized CRISPR/Cas gRNAs for functional interrogations in the coding and noncoding genome. eLife, 8, pii: e42549.





Di Rita A, Peschiaroli A, D Acunzo P, Strobbe D, Hu Z, Gruber J, Nygaard M, Lambrughi M, Melino G, Papaleo E, Dengjel J, El Alaoui S, Campanella M, Dötsch V, Rogov VV, Strappazzon F, Cecconi F. HUWE1 E3 ligase promotes PINK1/PARKIN-independent mitophagy by regulating AMBRA1 activation via IKKα. Nat Commun. 2018 Sep 14;9(1):3755. doi: 10.1038/s41467-018-05722-3. PubMed PMID: 30217973; PubMed Central PMCID: PMC6138665.


Kniss A, Kazemi S, Löhr F, Berger M, Rogov VV, Güntert P, Sommer T, Jarosch E, Dötsch V. Structural investigation of glycan recognition by the ERAD quality control lectin Yos9. J Biomol NMR. 2018 Jul 31. doi: 10.1007/s10858-018-0201-6. [Epub ahead of print] PubMed PMID: 30066206.


Meyer N, Zielke S, Michaelis JB, Linder B, Warnsmann V, Rakel S, Osiewacz HD, Fulda S, Mittelbronn M, Münch C, Behrends C, Kögel D. AT 101 induces early mitochondrial dysfunction and HMOX1 (heme oxygenase 1) to trigger mitophagic cell death in glioma cells. Autophagy. 2018;14(10):1693-1709. doi: 10.1080/15548627.2018.1476812. Epub 2018 Jul 21. PubMed PMID: 29938581; PubMed Central PMCID: PMC6135628.


Phelan JD, Young RM, Webster DE, Roulland S, Wright GW, Kasbekar M, Shaffer AL 3rd, Ceribelli M, Wang JQ, Schmitz R, Nakagawa M, Bachy E, Huang DW, Ji Y, Chen L, Yang Y, Zhao H, Yu X, Xu W, Palisoc MM, Valadez RR, Davies-Hill T, Wilson WH, Chan WC, Jaffe ES, Gascoyne RD, Campo E, Rosenwald A, Ott G, Delabie J, Rimsza LM, Rodriguez FJ, Estephan F, Holdhoff M, Kruhlak MJ, Hewitt SM, Thomas CJ, Pittaluga S, Oellerich T, Staudt LM. A multiprotein supercomplex controlling oncogenic signalling in lymphoma. Nature. 2018 Aug;560(7718):387-391. doi: 10.1038/s41586-018-0290-0. Epub 2018 Jun 20. PubMed PMID: 29925955.


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Bhogaraju S, Kalayil S, Liu Y, Bonn F, Colby T, Matic I, Dikic I. Phosphoribosylation of Ubiquitin Promotes Serine Ubiquitination and Impairs Conventional Ubiquitination. Cell. 2016 Dec 1;167(6):1636-1649.e13. doi: 10.1016/j.cell.2016.11.019. PubMed PMID: 27912065.


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