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  1. Article: Studying Autophagy in Zebrafish.

    Mathai, Benan John / Meijer, Annemarie H / Simonsen, Anne

    Cells

    2017  Volume 6, Issue 3

    Abstract: Autophagy is an evolutionarily conserved catabolic process which allows lysosomal degradation of complex cytoplasmic components into basic biomolecules that are recycled for further cellular use. Autophagy is critical for cellular homeostasis and for ... ...

    Abstract Autophagy is an evolutionarily conserved catabolic process which allows lysosomal degradation of complex cytoplasmic components into basic biomolecules that are recycled for further cellular use. Autophagy is critical for cellular homeostasis and for degradation of misfolded proteins and damaged organelles as well as intracellular pathogens. The role of autophagy in protection against age-related diseases and a plethora of other diseases is now coming to light; assisted by several divergent eukaryotic model systems ranging from yeast to mice. We here give an overview of different methods used to analyse autophagy in zebrafish-a relatively new model for studying autophagy-and briefly discuss what has been done so far and possible future directions.
    Language English
    Publishing date 2017-07-09
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2661518-6
    ISSN 2073-4409
    ISSN 2073-4409
    DOI 10.3390/cells6030021
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Studying Autophagy in Zebrafish

    Benan John Mathai / Annemarie H. Meijer / Anne Simonsen

    Cells, Vol 6, Iss 3, p

    2017  Volume 21

    Abstract: Autophagy is an evolutionarily conserved catabolic process which allows lysosomal degradation of complex cytoplasmic components into basic biomolecules that are recycled for further cellular use. Autophagy is critical for cellular homeostasis and for ... ...

    Abstract Autophagy is an evolutionarily conserved catabolic process which allows lysosomal degradation of complex cytoplasmic components into basic biomolecules that are recycled for further cellular use. Autophagy is critical for cellular homeostasis and for degradation of misfolded proteins and damaged organelles as well as intracellular pathogens. The role of autophagy in protection against age-related diseases and a plethora of other diseases is now coming to light; assisted by several divergent eukaryotic model systems ranging from yeast to mice. We here give an overview of different methods used to analyse autophagy in zebrafish—a relatively new model for studying autophagy—and briefly discuss what has been done so far and possible future directions.
    Keywords autophagy ; zebrafish ; GFP-Lc3 ; confocal microscopy ; mitophagy ; aggrephagy ; xenophagy ; Biology (General) ; QH301-705.5
    Language English
    Publishing date 2017-07-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  3. Article ; Online: NIPSNAP1 and NIPSNAP2 act as "eat me" signals to allow sustained recruitment of autophagy receptors during mitophagy.

    Abudu, Yakubu Princely / Pankiv, Serhiy / Mathai, Benan John / Lamark, Trond / Johansen, Terje / Simonsen, Anne

    Autophagy

    2019  Volume 15, Issue 10, Page(s) 1845–1847

    Abstract: Removal of damaged mitochondria is vital for cellular homeostasis especially in non-dividing cells, like neurons. Damaged mitochondria that cannot be repaired by the ubiquitin-proteasomal system are cleared by a form of selective autophagy known as ... ...

    Abstract Removal of damaged mitochondria is vital for cellular homeostasis especially in non-dividing cells, like neurons. Damaged mitochondria that cannot be repaired by the ubiquitin-proteasomal system are cleared by a form of selective autophagy known as mitophagy. Following damage, mitochondria become labelled with 'eat-me' signals that selectively determine their degradation. Recently, we identified the mitochondrial matrix proteins, NIPSNAP1 (nipsnap homolog 1) and NIPSNAP2 as 'eat-me' signals for damaged mitochondria. NIPSNAP1 and NIPSNAP2 accumulate on the mitochondrial outer membrane following mitochondrial depolarization, recruiting autophagy receptors and adaptors, as well as human Atg8 (autophagy-related 8)-family proteins to facilitate mitophagy. The NIPSNAPs allow a sustained recruitment of SQSTM1-like receptors (SLRs) to ensure efficient mitophagy. Zebrafish lacking Nipsnap1 show decreased mitophagy in the brain coupled with increased ROS production, loss of dopaminergic neurons and strongly reduced locomotion.
    MeSH term(s) Animals ; Animals, Genetically Modified ; Autophagy ; Autophagy-Related Protein 8 Family/genetics ; Autophagy-Related Protein 8 Family/metabolism ; Autophagy-Related Proteins/metabolism ; Gene Knockout Techniques ; HeLa Cells ; Humans ; Intercellular Signaling Peptides and Proteins/physiology ; Intracellular Signaling Peptides and Proteins/physiology ; Membrane Proteins/physiology ; Mitophagy/genetics ; Protein Binding ; Sequestosome-1 Protein/chemistry ; Sequestosome-1 Protein/metabolism ; Signal Transduction/genetics ; Zebrafish
    Chemical Substances Autophagy-Related Protein 8 Family ; Autophagy-Related Proteins ; GABARAPL2 protein, human ; Intercellular Signaling Peptides and Proteins ; Intracellular Signaling Peptides and Proteins ; Membrane Proteins ; NIPSNAP1 protein, human ; NIPSNAP2 protein, human ; Sequestosome-1 Protein
    Language English
    Publishing date 2019-07-04
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2454135-7
    ISSN 1554-8635 ; 1554-8627
    ISSN (online) 1554-8635
    ISSN 1554-8627
    DOI 10.1080/15548627.2019.1637642
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: NIPSNAP1 and NIPSNAP2 Act as "Eat Me" Signals for Mitophagy.

    Princely Abudu, Yakubu / Pankiv, Serhiy / Mathai, Benan John / Håkon Lystad, Alf / Bindesbøll, Christian / Brenne, Hanne Britt / Yoke Wui Ng, Matthew / Thiede, Bernd / Yamamoto, Ai / Mutugi Nthiga, Thaddaeus / Lamark, Trond / Esguerra, Camila V / Johansen, Terje / Simonsen, Anne

    Developmental cell

    2019  Volume 49, Issue 4, Page(s) 509–525.e12

    Abstract: The clearance of damaged or dysfunctional mitochondria by selective autophagy (mitophagy) is important for cellular homeostasis and prevention of disease. Our understanding of the mitochondrial signals that trigger their recognition and targeting by ... ...

    Abstract The clearance of damaged or dysfunctional mitochondria by selective autophagy (mitophagy) is important for cellular homeostasis and prevention of disease. Our understanding of the mitochondrial signals that trigger their recognition and targeting by mitophagy is limited. Here, we show that the mitochondrial matrix proteins 4-Nitrophenylphosphatase domain and non-neuronal SNAP25-like protein homolog 1 (NIPSNAP1) and NIPSNAP2 accumulate on the mitochondria surface upon mitochondrial depolarization. There, they recruit proteins involved in selective autophagy, including autophagy receptors and ATG8 proteins, thereby functioning as an "eat me" signal for mitophagy. NIPSNAP1 and NIPSNAP2 have a redundant function in mitophagy and are predominantly expressed in different tissues. Zebrafish lacking a functional Nipsnap1 display reduced mitophagy in the brain and parkinsonian phenotypes, including loss of tyrosine hydroxylase (Th1)-positive dopaminergic (DA) neurons, reduced motor activity, and increased oxidative stress.
    MeSH term(s) Adaptor Proteins, Signal Transducing/metabolism ; Animals ; Autophagy/physiology ; Autophagy-Related Protein 8 Family/metabolism ; Carrier Proteins/metabolism ; HEK293 Cells ; HeLa Cells ; Humans ; Intercellular Signaling Peptides and Proteins/metabolism ; Intracellular Signaling Peptides and Proteins/metabolism ; Membrane Proteins/metabolism ; Microtubule-Associated Proteins/metabolism ; Mitochondria/metabolism ; Mitochondrial Proteins/metabolism ; Mitophagy/physiology ; Neurons/metabolism ; Protein Binding ; RNA-Binding Proteins/metabolism ; Sequestosome-1 Protein/metabolism ; Transcription Factors/metabolism ; Ubiquitin-Protein Ligases/metabolism ; Zebrafish ; Zebrafish Proteins/metabolism
    Chemical Substances Adaptor Proteins, Signal Transducing ; Autophagy-Related Protein 8 Family ; Carrier Proteins ; Intercellular Signaling Peptides and Proteins ; Intracellular Signaling Peptides and Proteins ; Membrane Proteins ; Microtubule-Associated Proteins ; Mitochondrial Proteins ; NIPSNAP1 protein, human ; NIPSNAP2 protein, human ; P62 protein, human ; RNA-Binding Proteins ; SQSTM1 protein, human ; Sequestosome-1 Protein ; Transcription Factors ; WDFY3 protein, human ; Zebrafish Proteins ; Ubiquitin-Protein Ligases (EC 2.3.2.27)
    Language English
    Publishing date 2019-04-11
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2054967-2
    ISSN 1878-1551 ; 1534-5807
    ISSN (online) 1878-1551
    ISSN 1534-5807
    DOI 10.1016/j.devcel.2019.03.013
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5742: Show issues Location:
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    Jg. 1995 - 2021: Lesesall (2.OG)
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    Zs.MG 76: Show issues

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  5. Article ; Online: Genome-wide association study for type 2 diabetes in Indians identifies a new susceptibility locus at 2q21.

    Tabassum, Rubina / Chauhan, Ganesh / Dwivedi, Om Prakash / Mahajan, Anubha / Jaiswal, Alok / Kaur, Ismeet / Bandesh, Khushdeep / Singh, Tejbir / Mathai, Benan John / Pandey, Yogesh / Chidambaram, Manickam / Sharma, Amitabh / Chavali, Sreenivas / Sengupta, Shantanu / Ramakrishnan, Lakshmi / Venkatesh, Pradeep / Aggarwal, Sanjay K / Ghosh, Saurabh / Prabhakaran, Dorairaj /
    Srinath, Reddy K / Saxena, Madhukar / Banerjee, Monisha / Mathur, Sandeep / Bhansali, Anil / Shah, Viral N / Madhu, Sri Venkata / Marwaha, Raman K / Basu, Analabha / Scaria, Vinod / McCarthy, Mark I / Venkatesan, Radha / Mohan, Viswanathan / Tandon, Nikhil / Bharadwaj, Dwaipayan

    Diabetes

    2012  Volume 62, Issue 3, Page(s) 977–986

    Abstract: Indians undergoing socioeconomic and lifestyle transitions will be maximally affected by epidemic of type 2 diabetes (T2D). We conducted a two-stage genome-wide association study of T2D in 12,535 Indians, a less explored but high-risk group. We ... ...

    Abstract Indians undergoing socioeconomic and lifestyle transitions will be maximally affected by epidemic of type 2 diabetes (T2D). We conducted a two-stage genome-wide association study of T2D in 12,535 Indians, a less explored but high-risk group. We identified a new type 2 diabetes-associated locus at 2q21, with the lead signal being rs6723108 (odds ratio 1.31; P = 3.32 × 10⁻⁹). Imputation analysis refined the signal to rs998451 (odds ratio 1.56; P = 6.3 × 10⁻¹²) within TMEM163 that encodes a probable vesicular transporter in nerve terminals. TMEM163 variants also showed association with decreased fasting plasma insulin and homeostatic model assessment of insulin resistance, indicating a plausible effect through impaired insulin secretion. The 2q21 region also harbors RAB3GAP1 and ACMSD; those are involved in neurologic disorders. Forty-nine of 56 previously reported signals showed consistency in direction with similar effect sizes in Indians and previous studies, and 25 of them were also associated (P < 0.05). Known loci and the newly identified 2q21 locus altogether explained 7.65% variance in the risk of T2D in Indians. Our study suggests that common susceptibility variants for T2D are largely the same across populations, but also reveals a population-specific locus and provides further insights into genetic architecture and etiology of T2D.
    MeSH term(s) Aged ; Asians ; Chromosomes, Human, Pair 2/genetics ; Diabetes Mellitus, Type 2/genetics ; Diabetes Mellitus, Type 2/metabolism ; Genetic Loci ; Genetic Predisposition to Disease ; Genome-Wide Association Study ; Humans ; India ; Insulin Resistance ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Middle Aged ; Nerve Tissue Proteins/genetics ; Nerve Tissue Proteins/metabolism ; Polymorphism, Single Nucleotide ; Whites
    Chemical Substances Membrane Proteins ; Nerve Tissue Proteins ; TMEM163 protein, human
    Language English
    Publishing date 2012-12-03
    Publishing country United States
    Document type Journal Article ; Meta-Analysis ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 80085-5
    ISSN 1939-327X ; 0012-1797
    ISSN (online) 1939-327X
    ISSN 0012-1797
    DOI 10.2337/db12-0406
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Uh III Zs.175: Show issues Location:
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