A citation-based method for searching scientific literature

Alaa Eskandrani, Amal AlHashem, El-Sayed Ali, Saad AlShahwan, Kalthoum Tlili, Khaled Hundallah, Brahim Tabarki. Pediatr Neurol 2017
Times Cited: 13







List of co-cited articles
51 articles co-cited >1



Times Cited
  Times     Co-cited
Similarity


Whole-exome sequencing identifies homozygous AFG3L2 mutations in a spastic ataxia-neuropathy syndrome linked to mitochondrial m-AAA proteases.
Tyler Mark Pierson, David Adams, Florian Bonn, Paola Martinelli, Praveen F Cherukuri, Jamie K Teer, Nancy F Hansen, Pedro Cruz, James C Mullikin For The Nisc Comparative Sequencing Program, Robert W Blakesley,[...]. PLoS Genet 2011
137
76

Mutations in the mitochondrial protease gene AFG3L2 cause dominant hereditary ataxia SCA28.
Daniela Di Bella, Federico Lazzaro, Alfredo Brusco, Massimo Plumari, Giorgio Battaglia, Annalisa Pastore, Adele Finardi, Claudia Cagnoli, Filippo Tempia, Marina Frontali,[...]. Nat Genet 2010
210
61

AFG3L2 supports mitochondrial protein synthesis and Purkinje cell survival.
Eva R Almajan, Ricarda Richter, Lars Paeger, Paola Martinelli, Esther Barth, Thorsten Decker, Nils-Göran Larsson, Peter Kloppenburg, Thomas Langer, Elena I Rugarli. J Clin Invest 2012
72
46

The m-AAA Protease Associated with Neurodegeneration Limits MCU Activity in Mitochondria.
Tim König, Simon E Tröder, Kavya Bakka, Anne Korwitz, Ricarda Richter-Dennerlein, Philipp A Lampe, Maria Patron, Mareike Mühlmeister, Sergio Guerrero-Castillo, Ulrich Brandt,[...]. Mol Cell 2016
92
38

The mitochondrial protease AFG3L2 is essential for axonal development.
Francesca Maltecca, Asadollah Aghaie, David G Schroeder, Laura Cassina, Benjamin A Taylor, Sandra J Phillips, Mariachiara Malaguti, Stefano Previtali, Jean-Louis Guénet, Angelo Quattrini,[...]. J Neurosci 2008
78
38

Haploinsufficiency of AFG3L2, the gene responsible for spinocerebellar ataxia type 28, causes mitochondria-mediated Purkinje cell dark degeneration.
Francesca Maltecca, Raffaella Magnoni, Federica Cerri, Gregory A Cox, Angelo Quattrini, Giorgio Casari. J Neurosci 2009
76
38

A recurrent de novo mutation in KCNC1 causes progressive myoclonus epilepsy.
Mikko Muona, Samuel F Berkovic, Leanne M Dibbens, Karen L Oliver, Snezana Maljevic, Marta A Bayly, Tarja Joensuu, Laura Canafoglia, Silvana Franceschetti, Roberto Michelucci,[...]. Nat Genet 2015
152
38

Missense mutations in the AFG3L2 proteolytic domain account for ∼1.5% of European autosomal dominant cerebellar ataxias.
Claudia Cagnoli, Giovanni Stevanin, Alessandro Brussino, Marco Barberis, Cecilia Mancini, Russell L Margolis, Susan E Holmes, Marcello Nobili, Sylvie Forlani, Sergio Padovan,[...]. Hum Mutat 2010
59
38

Spastic paraplegia and OXPHOS impairment caused by mutations in paraplegin, a nuclear-encoded mitochondrial metalloprotease.
G Casari, M De Fusco, S Ciarmatori, M Zeviani, M Mora, P Fernandez, G De Michele, A Filla, S Cocozza, R Marconi,[...]. Cell 1998
600
30

The m-AAA protease defective in hereditary spastic paraplegia controls ribosome assembly in mitochondria.
Mark Nolden, Sarah Ehses, Mirko Koppen, Andrea Bernacchia, Elena I Rugarli, Thomas Langer. Cell 2005
276
30

Variable and tissue-specific subunit composition of mitochondrial m-AAA protease complexes linked to hereditary spastic paraplegia.
Mirko Koppen, Metodi D Metodiev, Giorgio Casari, Elena I Rugarli, Thomas Langer. Mol Cell Biol 2007
133
30

Early onset and slow progression of SCA28, a rare dominant ataxia in a large four-generation family with a novel AFG3L2 mutation.
Ulf Edener, Janine Wöllner, Ute Hehr, Zacharias Kohl, Stefan Schilling, Friedmar Kreuz, Peter Bauer, Veronica Bernard, Gabriele Gillessen-Kaesbach, Christine Zühlke. Eur J Hum Genet 2010
39
30

m-AAA proteases, mitochondrial calcium homeostasis and neurodegeneration.
Maria Patron, Hans-Georg Sprenger, Thomas Langer. Cell Res 2018
45
30

A novel mutation of AFG3L2 might cause dominant optic atrophy in patients with mild intellectual disability.
Majida Charif, Agathe Roubertie, Sara Salime, Sonia Mamouni, Cyril Goizet, Christian P Hamel, Guy Lenaers. Front Genet 2015
26
30

Spinocerebellar Ataxia Type 28-Phenotypic and Molecular Characterization of a Family with Heterozygous and Compound-Heterozygous Mutations in AFG3L2.
Sinem Tunc, Marija Dulovic-Mahlow, Hauke Baumann, Magdalena Khira Baaske, Magdalena Jahn, Johanna Junker, Alexander Münchau, Norbert Brüggemann, Katja Lohmann. Cerebellum 2019
7
57

Purkinje neuron Ca2+ influx reduction rescues ataxia in SCA28 model.
Francesca Maltecca, Elisa Baseggio, Francesco Consolato, Davide Mazza, Paola Podini, Samuel M Young, Ilaria Drago, Ben A Bahr, Aldamaria Puliti, Franca Codazzi,[...]. J Clin Invest 2015
46
23

The i-AAA protease YME1L and OMA1 cleave OPA1 to balance mitochondrial fusion and fission.
Ruchika Anand, Timothy Wai, Michael J Baker, Nikolay Kladt, Astrid C Schauss, Elena Rugarli, Thomas Langer. J Cell Biol 2014
385
23

New roles for mitochondrial proteases in health, ageing and disease.
Pedro M Quirós, Thomas Langer, Carlos López-Otín. Nat Rev Mol Cell Biol 2015
284
23

SCA28: Novel Mutation in the AFG3L2 Proteolytic Domain Causes a Mild Cerebellar Syndrome with Selective Type-1 Muscle Fiber Atrophy.
Kirsten Svenstrup, Troels Tolstrup Nielsen, Frederik Aidt, Nina Rostgaard, Morten Duno, Flemming Wibrand, Tua Vinther-Jensen, Ian Law, John Vissing, Peter Roos,[...]. Cerebellum 2017
11
27

A novel missense mutation in AFG3L2 associated with late onset and slow progression of spinocerebellar ataxia type 28.
Anna Mareike Löbbe, Jun-Suk Kang, Rüdiger Hilker, Holger Hackstein, Ulrich Müller, Dagmar Nolte. J Mol Neurosci 2014
18
23

Partial deletion of AFG3L2 causing spinocerebellar ataxia type 28.
Katrien Smets, Tine Deconinck, Jonathan Baets, Anne Sieben, Jean-Jacques Martin, Iris Smouts, Shuaiyu Wang, Franco Taroni, Daniela Di Bella, Wim Van Hecke,[...]. Neurology 2014
19
23

Spinocerebellar ataxia 28: a novel AFG3L2 mutation in a German family with young onset, slow progression and saccadic slowing.
Christine Zühlke, Barbara Mikat, Dagmar Timmann, Dagmar Wieczorek, Gabriele Gillessen-Kaesbach, Katrin Bürk. Cerebellum Ataxias 2015
15
23

SCA28, a novel form of autosomal dominant cerebellar ataxia on chromosome 18p11.22-q11.2.
Claudia Cagnoli, Caterina Mariotti, Franco Taroni, Marco Seri, Alessandro Brussino, Chiara Michielotto, Marina Grisoli, Daniela Di Bella, Nicola Migone, Cinzia Gellera,[...]. Brain 2006
82
23

Neurocognitive Characterization of an SCA28 Family Caused by a Novel AFG3L2 Gene Mutation.
Laszlo Szpisjak, Viola L Nemeth, Noemi Szepfalusi, Denes Zadori, Zoltan Maroti, Tibor Kalmar, Laszlo Vecsei, Peter Klivenyi. Cerebellum 2017
6
50

Standards and guidelines for the interpretation of sequence variants: a joint consensus recommendation of the American College of Medical Genetics and Genomics and the Association for Molecular Pathology.
Sue Richards, Nazneen Aziz, Sherri Bale, David Bick, Soma Das, Julie Gastier-Foster, Wayne W Grody, Madhuri Hegde, Elaine Lyon, Elaine Spector,[...]. Genet Med 2015
15

Quality control of mitochondrial protein synthesis is required for membrane integrity and cell fitness.
Uwe Richter, Taina Lahtinen, Paula Marttinen, Fumi Suomi, Brendan J Battersby. J Cell Biol 2015
52
15

The matrix peptide exporter HAF-1 signals a mitochondrial UPR by activating the transcription factor ZC376.7 in C. elegans.
Cole M Haynes, Yun Yang, Steven P Blais, Thomas A Neubert, David Ron. Mol Cell 2010
327
15


AAA+ proteases: ATP-fueled machines of protein destruction.
Robert T Sauer, Tania A Baker. Annu Rev Biochem 2011
467
15

Loss of the m-AAA protease subunit AFG₃L₂ causes mitochondrial transport defects and tau hyperphosphorylation.
Arun Kumar Kondadi, Shuaiyu Wang, Sara Montagner, Nikolay Kladt, Anne Korwitz, Paola Martinelli, David Herholz, Michael J Baker, Astrid C Schauss, Thomas Langer,[...]. EMBO J 2014
46
15

Structure of the mitochondrial inner membrane AAA+ protease YME1 gives insight into substrate processing.
Cristina Puchades, Anthony J Rampello, Mia Shin, Christopher J Giuliano, R Luke Wiseman, Steven E Glynn, Gabriel C Lander. Science 2017
107
15

Stress-induced OMA1 activation and autocatalytic turnover regulate OPA1-dependent mitochondrial dynamics.
Michael J Baker, Philipp A Lampe, Diana Stojanovski, Anne Korwitz, Ruchika Anand, Takashi Tatsuta, Thomas Langer. EMBO J 2014
165
15


Respiratory dysfunction by AFG3L2 deficiency causes decreased mitochondrial calcium uptake via organellar network fragmentation.
Francesca Maltecca, Diego De Stefani, Laura Cassina, Francesco Consolato, Michal Wasilewski, Luca Scorrano, Rosario Rizzuto, Giorgio Casari. Hum Mol Genet 2012
40
15

Regulation of OPA1 processing and mitochondrial fusion by m-AAA protease isoenzymes and OMA1.
Sarah Ehses, Ines Raschke, Giuseppe Mancuso, Andrea Bernacchia, Stefan Geimer, Daniel Tondera, Jean-Claude Martinou, Benedikt Westermann, Elena I Rugarli, Thomas Langer. J Cell Biol 2009
372
15

Electron cryomicroscopy structure of a membrane-anchored mitochondrial AAA protease.
Sukyeong Lee, Steffen Augustin, Takashi Tatsuta, Florian Gerdes, Thomas Langer, Francis T F Tsai. J Biol Chem 2011
43
15

A novel frameshift mutation in the AFG3L2 gene in a patient with spinocerebellar ataxia.
Zuzana Musova, Michaela Kaiserova, Eva Kriegova, Regina Fillerova, Peter Vasovcak, Alena Santava, Katerina Mensikova, Alena Zumrova, Anna Krepelova, Zdenek Sedlacek,[...]. Cerebellum 2014
15
15


Identification and characterization of AFG3L2, a novel paraplegin-related gene.
S Banfi, M T Bassi, G Andolfi, A Marchitiello, S Zanotta, A Ballabio, G Casari, B Franco. Genomics 1999
60
15

Genetic interaction between the m-AAA protease isoenzymes reveals novel roles in cerebellar degeneration.
Paola Martinelli, Veronica La Mattina, Andrea Bernacchia, Raffaella Magnoni, Federica Cerri, Gregory Cox, Angelo Quattrini, Giorgio Casari, Elena I Rugarli. Hum Mol Genet 2009
41
15

A method and server for predicting damaging missense mutations.
Ivan A Adzhubei, Steffen Schmidt, Leonid Peshkin, Vasily E Ramensky, Anna Gerasimova, Peer Bork, Alexey S Kondrashov, Shamil R Sunyaev. Nat Methods 2010
15

A panel study on patients with dominant cerebellar ataxia highlights the frequency of channelopathies.
Marie Coutelier, Giulia Coarelli, Marie-Lorraine Monin, Juliette Konop, Claire-Sophie Davoine, Christelle Tesson, Rémi Valter, Mathieu Anheim, Anthony Behin, Giovanni Castelnovo,[...]. Brain 2017
56
15


Recessive mutations in VPS13D cause childhood onset movement disorders.
Julie Gauthier, Inge A Meijer, Davor Lessel, Niccolò E Mencacci, Dimitri Krainc, Maja Hempel, Konstantinos Tsiakas, Holger Prokisch, Elsa Rossignol, Margaret H Helm,[...]. Ann Neurol 2018
51
15

Mitochondrial Quality Control Proteases in Neuronal Welfare.
Roman M Levytskyy, Edward M Germany, Oleh Khalimonchuk. J Neuroimmune Pharmacol 2016
20
15

Mutations in VPS13D lead to a new recessive ataxia with spasticity and mitochondrial defects.
Eunju Seong, Ryan Insolera, Marija Dulovic, Erik-Jan Kamsteeg, Joanne Trinh, Norbert Brüggemann, Erin Sandford, Sheng Li, Ayse Bilge Ozel, Jun Z Li,[...]. Ann Neurol 2018
63
15

Non-syndromic isolated dominant optic atrophy caused by the p.R468C mutation in the AFG3 like matrix AAA peptidase subunit 2 gene.
Davide Colavito, Veronica Maritan, Agnese Suppiej, Elda Del Giudice, Monica Mazzarolo, Stefania Miotto, Sofia Farina, Maurizio Dalle Carbonare, Stefano Piermarocchi, Alberta Leon. Biomed Rep 2017
12
16


Pathogenic variants in the AFG3L2 proteolytic domain cause SCA28 through haploinsufficiency and proteostatic stress-driven OMA1 activation.
Susanna Tulli, Andrea Del Bondio, Valentina Baderna, Davide Mazza, Franca Codazzi, Tyler Mark Pierson, Alessandro Ambrosi, Dagmar Nolte, Cyril Goizet, Camilo Toro,[...]. J Med Genet 2019
10
20

Unique Structural Features of the Mitochondrial AAA+ Protease AFG3L2 Reveal the Molecular Basis for Activity in Health and Disease.
Cristina Puchades, Bojian Ding, Albert Song, R Luke Wiseman, Gabriel C Lander, Steven E Glynn. Mol Cell 2019
29
15


Co-cited is the co-citation frequency, indicating how many articles cite the article together with the query article. Similarity is the co-citation as percentage of the times cited of the query article or the article in the search results, whichever is the lowest. These numbers are calculated for the last 100 citations when articles are cited more than 100 times.