64 research outputs found
Retinoic Acid Functions as a Key GABAergic Differentiation Signal in the Basal Ganglia
- Author
- A Molotkov
- A Pierani
- A. M Maroof
- C Chatzi
- C Chatzi
- C Horton
- C Metin
- C Strubing
- C. P Wonders
- C. P Wonders
- Christina Chatzi
- D Smith
- D. A Lewis
- D. G Wilkinson
- E Ruberte
- E Wagner
- F. A Mic
- F. A Mic
- F. M Benes
- F. T Merkle
- G Bain
- G Duester
- G. B Potter
- Gregg Duester
- H Li
- H Marshall
- H Toresson
- H Wichterle
- H Wichterle
- H Wichterle
- J Ericson
- J Stenman
- J. A Siegenthaler
- J. A Thomson
- J. E Crandall
- J. L Rubenstein
- J. M Tepper
- K Zarbalis
- K Zarbalis
- K. F Liem Jr
- K. M Young
- L Danglot
- L. L Sandell
- M Alvarez-Dolado
- M Kim
- M Kohwi
- M Maden
- M Olsson
- M Olsson
- M Olsson
- M Wagner
- M. A Kane
- N Molotkova
- N Moreno
- N. E Rawson
- O Marin
- O Marin
- P. S Kalanithi
- Q Xu
- R Mollard
- R. J Ferland
- R. R Waclaw
- R. R Waclaw
- S Shen
- S. A Anderson
- S. A Anderson
- S. C Baraban
- S. J Pleasure
- S. L McIntire
- T. W Deacon
- Theo D. Palmer
- Thomas Brade
- V Dupe
- V. V Rymar
- W. L Liao
- X Fan
- X Zhao
- X Zhao
- Y Okada
- Publication venue
- Public Library of Science
- Publication date
- 01/01/2011
- Field of study
Retinoic acid (RA) is essential for the generation of GABAergic inhibitory neurons in the mouse forebrain, and RA treatment of embryonic stem cells induces the production of GABAergic neurons
A Transient Transgenic RNAi Strategy for Rapid Characterization of Gene Function during Embryonic Development
- Author
- A Kasarskis
- A Nagy
- A Pfeifer
- A Reynolds
- A Wilber
- AD Heggestad
- AJ Dupuy
- AJ Dupuy
- AJ Dupuy
- AM Geurts
- AM Geurts
- BC Bjork
- BJ Herron
- Bryan C. Bjork
- C Miskey
- CW Park
- DA Rubinson
- David R. Beier
- F Park
- Ferenc Mueller
- GJ Hannon
- Haiyan Qiu
- JJ Sager
- K Yusa
- K Zarbalis
- L Mates
- M Kirilov
- MT McManus
- MW Ferguson
- N Mochizuki
- N Wang
- O Singer
- P Sandy
- Peter Sandy
- PH Olsen
- PI Makinen
- PJ Paddison
- Q Yu
- R Ikeda
- S Ding
- SA Miller
- Sally A. Camper
- SC Wu
- Shannon W. Davis
- SM Elbashir
- Stuart Orkin
- Thomas L. Saunders
- TM Hyatt
- TR Brummelkamp
- VW Keng
- Y Chai
- Yuko Fujiwara
- Publication venue
- Public Library of Science
- Publication date
- 01/05/2010
- Field of study
RNA interference (RNAi) is a powerful strategy for studying the phenotypic consequences of reduced gene expression levels in model systems. To develop a method for the rapid characterization of the developmental consequences of gene dysregulation, we tested the use of RNAi for âtransient transgenicâ knockdown of mRNA in mouse embryos. These methods included lentiviral infection as well as transposition using the Sleeping Beauty (SB) and PiggyBac (PB) transposable element systems. This approach can be useful for phenotypic validation of putative mutant loci, as we demonstrate by confirming that knockdown of Prdm16 phenocopies the ENU-induced cleft palate (CP) mutant, csp1. This strategy is attractive as an alternative to gene targeting in embryonic stem cells, as it is simple and yields phenotypic information in a matter of weeks. Of the three methodologies tested, the PB transposon system produced high numbers of transgenic embryos with the expected phenotype, demonstrating its utility as a screening method
Loss of Col3a1, the Gene for Ehlers-Danlos Syndrome Type IV, Results in Neocortical Dyslamination
- Author
- A De Arcangelis
- A Niewmierzycka
- A Plancke
- BJ Molyneaux
- BS Chang
- C Englund
- C Labelle-Dumais
- D Graus-Porta
- DE Michele
- DJ Prockop
- DP Germain
- DS Rice
- E Georges-Labouesse
- E Parrini
- E Vuorio
- EC Olson
- EH Epstein Jr
- F Tissir
- FM Pope
- H Kuivaniemi
- HE Beggs
- J Sievers
- K Zarbalis
- KD Little
- Lin Mei
- M Costell
- M Nieto
- MD Henry
- N Bahi-Buisson
- N Haubst
- Natalie Strokes
- P Bornstein
- P Rakic
- R Barresi
- R Luo
- RA Williamson
- Rong Luo
- RS Piezzi
- S Kontusaari
- S Levy
- S Li
- Shihong Li
- Sung-Jin Jeong
- T Inoue
- U Schwarze
- W Halfter
- X Liu
- X Piao
- X Piao
- X Piao
- Xianhua Piao
- Publication venue
- Public Library of Science
- Publication date
- 03/01/2012
- Field of study
It has recently been discovered that Collagen III, the encoded protein of the type IV Ehlers-Danlos Syndrome (EDS) gene, is one of the major constituents of the pial basement membrane (BM) and serves as the ligand for GPR56. Mutations in GPR56 cause a severe human brain malformation called bilateral frontoparietal polymicrogyria, in which neurons transmigrate through the BM causing severe mental retardation and frequent seizures. To further characterize the brain phenotype of Col3a1 knockout mice, we performed a detailed histological analysis. We observed a cobblestone-like cortical malformation, with BM breakdown and marginal zone heterotopias in Col3a1â/â mouse brains. Surprisingly, the pial BM appeared intact at early stages of development but starting as early as embryonic day (E) 11.5, prominent BM defects were observed and accompanied by neuronal overmigration. Although collagen III is expressed in meningeal fibroblasts (MFs), Col3a1â/â MFs present no obvious defects. Furthermore, the expression and posttranslational modification of α-dystroglycan was undisturbed in Col3a1â/â mice. Based on the previous finding that mutations in COL3A1 cause type IV EDS, our study indicates a possible common pathological pathway linking connective tissue diseases and brain malformations
Bmp7 Regulates the Survival, Proliferation, and Neurogenic Properties of Neural Progenitor Cells during Corticogenesis in the Mouse
- Author
- A Niewmierzycka
- A Nohe
- Aikaterini Segklia
- AT Dudley
- C Englund
- C Fode
- C Leung-Hagesteijn
- C Schuurmans
- D Chen
- D Colak
- D Park
- Daniel Graf
- Danny Huylebroeck
- DO Wagner
- DW Hampton
- E Gazzerro
- E Remboutsika
- Elke Stappers
- Eumorphia Remboutsika
- Eve Seuntjens
- F Aboitiz
- G D'Arcangelo
- G D'Arcangelo
- G Fishell
- G Luo
- G Perides
- H Asada
- J Massague
- J Nickel
- JA Ortega
- JA Siegenthaler
- Jialin Charles Zheng
- JM Hebert
- K Zarbalis
- KJ Lee
- M Elkouris
- M Gotz
- M Gotz
- M Kleber
- M Leid
- M Ota
- M Yanagisawa
- Maximilianos Elkouris
- MJ Solloway
- MK Lehtinen
- Q Ma
- R Radakovits
- R Scardigli
- RE Godin
- S Cox
- S Falk
- SA Bayer
- SC Noctor
- SC Noctor
- SE Creuzet
- SM Kolk
- Sotiris Tsalavos
- SR Hutton
- T Yabe
- Thimios A. Mitsiadis
- V Borrell
- V Tarabykin
- V Zouvelou
- WA Gomes
- YX Li
- Publication venue
- Public Library of Science
- Publication date
- 01/01/2012
- Field of study
Bone morphogenetic proteins (BMPs) are considered important regulators of neural development. However, results mainly from a wide set of in vitro gain-of-function experiments are conflicting since these show that BMPs can act either as inhibitors or promoters of neurogenesis. Here, we report a specific and non-redundant role for BMP7 in cortical neurogenesis in vivo using knockout mice. Bmp7 is produced in regions adjacent to the developing cortex; the hem, meninges, and choroid plexus, and can be detected in the cerebrospinal fluid. Bmp7 deletion results in reduced cortical thickening, impaired neurogenesis, and loss of radial glia attachment to the meninges. Subsequent in vitro analyses of E14.5 cortical cells revealed that lack of Bmp7 affects neural progenitor cells, evidenced by their reduced proliferation, survival and self-renewal capacity. Addition of BMP7 was able to rescue these proliferation and survival defects. In addition, at the developmental stage E14.5 Bmp7 was also required to maintain Ngn2 expression in the subventricular zone. These data demonstrate a novel role for Bmp7 in the embryonic mouse cortex: Bmp7 nurtures radial glia cells and regulates fundamental properties of neural progenitor cells that subsequently affect Ngn2-dependent neurogenesis
The Ciliogenic Transcription Factor RFX3 Regulates Early Midline Distribution of Guidepost Neurons Required for Corpus Callosum Development
- Author
- A Putoux
- André Goffinet
- Aouatef Ait-Lounis
- B Wang
- Belkacem Otsmane
- BG Rash
- BJ Molyneaux
- BP Piasecki
- Bénédicte Durand
- C Fode
- C Schuurmans
- Carine Benadiba
- CH Yorke Jr
- CĂ©cile Lebrand
- D Baas
- D Kamnasaran
- Dario Magnani
- Delphine Valloton
- DP Leone
- E Bonnafe
- E Elson
- EA Alcamo
- EA Grove
- EC Engle
- EE Storm
- G Minowada
- GO Ivy
- H Sasaki
- Homaira Nawabi
- HS Ozaki
- I Mason
- I Naruse
- J Silver
- J Silver
- J Thomas
- J Vierkotten
- JA Gorski
- JA Rosenfeld
- Jean-Pierre Hornung
- JL Badano
- JL Tobin
- JM Hebert
- JS Chu
- K Aoto
- K Zarbalis
- KM Smith
- L Zhuo
- Laurette Morlé
- LJ Richards
- LK Paul
- M Niquille
- M Rallu
- MA Willaredt
- Mathieu Niquille
- N Jovanov-Milosevic
- O Britanova
- P Dai
- PJ Blackshear
- Q Xu
- RM Fame
- RW Stottmann
- RX Moldrich
- S Garel
- S Garel
- S Kuschel
- SA Brugmann
- SC Goetz
- SE Creuzet
- SE Creuzet
- SR May
- T Shu
- T Shu
- T Shu
- T Theil
- Thomas Theil
- UB Schambra
- W Reith
- Walter Reith
- X Wen
- Y Furuta
- Publication venue
- Public Library of Science
- Publication date
- 01/01/2012
- Field of study
The corpus callosum (CC) is the major commissure that bridges the cerebral hemispheres. Agenesis of the CC is associated with human ciliopathies, but the origin of this default is unclear. Regulatory Factor X3 (RFX3) is a transcription factor involved in the control of ciliogenesis, and Rfx3âdeficient mice show several hallmarks of ciliopathies including leftâright asymmetry defects and hydrocephalus. Here we show that Rfx3âdeficient mice suffer from CC agenesis associated with a marked disorganisation of guidepost neurons required for axon pathfinding across the midline. Using transplantation assays, we demonstrate that abnormalities of the mutant midline region are primarily responsible for the CC malformation. Conditional genetic inactivation shows that RFX3 is not required in guidepost cells for proper CC formation, but is required before E12.5 for proper patterning of the cortical septal boundary and hence accurate distribution of guidepost neurons at later stages. We observe focused but consistent ectopic expression of Fibroblast growth factor 8 (Fgf8) at the rostro commissural plate associated with a reduced ratio of GLIoma-associated oncogene family zinc finger 3 (GLI3) repressor to activator forms. We demonstrate on brain explant cultures that ectopic FGF8 reproduces the guidepost neuronal defects observed in Rfx3 mutants. This study unravels a crucial role of RFX3 during early brain development by indirectly regulating GLI3 activity, which leads to FGF8 upregulation and ultimately to disturbed distribution of guidepost neurons required for CC morphogenesis. Hence, the RFX3 mutant mouse model brings novel understandings of the mechanisms that underlie CC agenesis in ciliopathies
Mutations in Zebrafish lrp2 Result in Adult-Onset Ocular Pathogenesis That Models Myopia and Other Risk Factors for Glaucoma
- Author
- A Bosco
- A Maggs
- A Mii
- A Rolls
- AC Morris
- AJ Udvadia
- AM Solouki
- Ava J. Udvadia
- B Stevens
- BA Link
- BP Buckingham
- BR Pober
- Brian A. Link
- C Lillo
- CE Fisher
- CG Becker
- CL Schlamp
- CR Gajera
- D Allcutt
- D Donnai
- D Fischer
- D Sun
- Daniel S. Wagner
- DC Otteson
- DL Moore
- E Carro
- EI Christensen
- EI Christensen
- G Thorleifsson
- GR Howell
- Gregory B. Willer
- H Kuhrt
- H Tanihara
- HA Quigley
- HA Quigley
- HJ Schluesener
- I Dabin
- I Soto
- J Colavincenzo
- J Koistinaho
- J Rymer
- Janey Wiggs
- Jason R. Willer
- JC Downs
- JR Koke
- K Stasi
- K Zarbalis
- KA Soules
- Kerry N. Veth
- KM Gehrs
- L Xu
- LX Zhou
- M Berkelaar
- M Murray
- M Murray
- M Takeda
- M Westerfield
- Mary C. Mullins
- Matthew P. Gray
- MB Veldman
- MG Anderson
- MH Kuehn
- MJ Ignatius
- MP Gray
- MP Villegas-Perez
- MV Boland
- N Patel
- NI Loyo-Berrios
- NN Osborne
- P Bormann
- P May
- PA Raymond
- PA Raymond
- PF Hitchcock
- PG Hysi
- PR Johns
- R Spoelgen
- RI Bloom
- Richard S. Smith
- RL Levine
- Ronald G. Gregg
- Ross F. Collery
- RT Libby
- RW Nickells
- RW Sperry
- S Kantarci
- S Roth
- S Thanos
- Simon W. M. John
- SK Doster
- SM Hammad
- SS Easter Jr
- SS Easter Jr
- SW John
- T Herdegen
- TE Willnow
- TL Young
- U Anzenberger
- U Dirnagl
- V Pernet
- W Zhang
- WN Charman
- X Liu
- Y Kamatani
- Publication venue
- Public Library of Science
- Publication date
- 01/01/2011
- Field of study
The glaucomas comprise a genetically complex group of retinal neuropathies that typically occur late in life and are characterized by progressive pathology of the optic nerve head and degeneration of retinal ganglion cells. In addition to age and family history, other significant risk factors for glaucoma include elevated intraocular pressure (IOP) and myopia. The complexity of glaucoma has made it difficult to model in animals, but also challenging to identify responsible genes. We have used zebrafish to identify a genetically complex, recessive mutant that shows risk factors for glaucoma including adult onset severe myopia, elevated IOP, and progressive retinal ganglion cell pathology. Positional cloning and analysis of a non-complementing allele indicated that non-sense mutations in low density lipoprotein receptor-related protein 2 (lrp2) underlie the mutant phenotype. Lrp2, previously named Megalin, functions as an endocytic receptor for a wide-variety of bioactive molecules including Sonic hedgehog, Bone morphogenic protein 4, retinol-binding protein, vitamin D-binding protein, and apolipoprotein E, among others. Detailed phenotype analyses indicated that as lrp2 mutant fish age, many individualsâbut not allâdevelop high IOP and severe myopia with obviously enlarged eye globes. This results in retinal stretch and prolonged stress to retinal ganglion cells, which ultimately show signs of pathogenesis. Our studies implicate altered Lrp2-mediated homeostasis as important for myopia and other risk factors for glaucoma in humans and establish a new genetic model for further study of phenotypes associated with this disease
Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)
- Author
- A. -G. Wu
- A. C. Ma
- A. K. Au
- Abdel-Aziz A. K.
- Abdelfatah S.
- Abdellatif M.
- Abdoli A.
- Abel S.
- Abeliovich H.
- Abildgaard M. H.
- Abudu Y. P.
- Acevedo-Arozena A.
- Adamopoulos I. E.
- Adeli K.
- Adolph T. E.
- Adornetto A.
- Aflaki E.
- Agam G.
- Agarwal A.
- Aggarwal B. B.
- Agnello M.
- Agostinis P.
- Agrewala J. N.
- Agrotis A.
- Aguilar P. V.
- Ahmad S. T.
- Ahmed Z. M.
- Ahumada-Castro U.
- Aits S.
- Aizawa S.
- Akkoc Y.
- Akoumianaki T.
- Akpinar H. A.
- Al-Abd A. M.
- Al-Akra L.
- Al-Gharaibeh A.
- Alaoui-Jamali M. A.
- Alberti S.
- Alcocer-Gomez E.
- Alessandri C.
- Ali M.
- Alim Al-Bari M. A.
- Aliwaini S.
- Alizadeh J.
- Almacellas E.
- Almasan A.
- Alonso A.
- Alonso G. D.
- Altan-Bonnet N.
- Altieri D. C.
- Alvarez E. M. C.
- Alves da Costa C.
- Alves S.
- Alzaharna M. M.
- Amadio M.
- Amantini C.
- Amaral C.
- Ambrosio S.
- Amer A. O.
- Ammanathan V.
- An Z.
- Andersen S. U.
- Andrabi S. A.
- Andrade-Silva M.
- Andres A. M.
- Angelini S.
- Ann D.
- Anozie U. C.
- Ansari M. Y.
- Antas P.
- Antebi A.
- Anton Z.
- Anwar T.
- Apetoh L.
- Apostolova N.
- Araki T.
- Araki Y.
- Arasaki K.
- Araujo W. L.
- Araya J.
- Arden C.
- Arevalo M. -A.
- Arguelles S.
- Arias E.
- Arikkath J.
- Arimoto H.
- Ariosa A. R.
- Armstrong-James D.
- Arnaune-Pelloquin L.
- Aroca A.
- Arroyo D. S.
- Arsov I.
- Artero R.
- Asaro D. M. L.
- Aschner M.
- Ashrafizadeh M.
- Ashur-Fabian O.
- Atanasov A. G.
- Auberger P.
- Auner H. W.
- Aurelian L.
- Autelli R.
- Avagliano L.
- Avalos Y.
- Aveic S.
- Aveleira C. A.
- Avin-Wittenberg T.
- Aydin Y.
- Ayton S.
- Ayyadevara S.
- Azzopardi M.
- B. C. B. Ko
- Baba M.
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- Baek A.
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- Bagetta G.
- Bagniewska-Zadworna A.
- Bai H.
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- Bairagi N.
- Baksi S.
- Balazadeh S.
- Balbi T.
- Baldari C. T.
- Balduini W.
- Ballabio A.
- Ballester M.
- Balzan R.
- Bandopadhyay R.
- Banerjee S.
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- Barila D.
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- Bellarosa C.
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- Benitez B. A.
- Benito-Cuesta I.
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- Bourgeois B.
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- Bozhkov P. V.
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- Bringer M. -A.
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- C. C. W. Ng
- C. H. Lo
- Cabas I.
- Cabrera-Benitez S.
- Cadwell K.
- Cai J.
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- Cai Q.
- Cairo M.
- Calbet J. A.
- Caldwell G. A.
- Caldwell K. A.
- Call J. A.
- Calvani R.
- Calvo A. C.
- Calvo-Rubio Barrera M.
- Camara N. O. S.
- Camonis J. H.
- Camougrand N.
- Campanella M.
- Campbell E. M.
- Campbell-Valois F. -X.
- Campello S.
- Campesi I.
- Campos J. C.
- Camuzard O.
- Cancino J.
- Candido de Almeida D.
- Canesi L.
- Caniggia I.
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- Cao B.
- Caraglia M.
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- Carchman E. H.
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- Cardenas C.
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- Cassioli C.
- Castillo E. F.
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- Castillo-Lluva S.
- Castoldi F.
- Castori M.
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- Castro-Caldas M.
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- Castro-Obregon S.
- Catz S. D.
- Cavadas C.
- Cavaliere F.
- Cavallini G.
- Cavinato M.
- Cayuela M. L.
- Cebollada Rica P.
- Cecarini V.
- Cecconi F.
- Cechowska-Pasko M.
- Cenci S.
- Ceperuelo-Mallafre V.
- Cerqueira J. J.
- Cerutti J. M.
- Cervia D.
- Cetintas V. B.
- Cetrullo S.
- Chae H. -J.
- Chagin A. S.
- Chai C. -Y.
- Chakrabarti G.
- Chakrabarti O.
- Chakraborty T.
- Chakraborty T.
- Chami M.
- Chamilos G.
- Chan D. W.
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- Publication venue
- 'Informa UK Limited'
- Publication date
- 01/01/2021
- Field of study
Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)1.
- Author
- Abdel-Aziz AK
- Abdelfatah S
- Abdellatif M
- Abdoli A
- Abel S
- Abeliovich H
- Abildgaard MH
- Abudu YP
- Acevedo-Arozena A
- Adamopoulos IE
- Adeli K
- Adolph TE
- Adornetto A
- Aflaki E
- Agam G
- Agarwal A
- Aggarwal BB
- Agnello M
- Agostinis P
- Agrewala JN
- Agrotis A
- Aguilar PV
- Ahmad ST
- Ahmed ZM
- Ahumada-Castro U
- Aits S
- Aizawa S
- Akkoc Y
- Akoumianaki T
- Akpinar HA
- Al-Abd AM
- Al-Akra L
- Al-Gharaibeh A
- Alaoui-Jamali MA
- Alberti S
- Alcocer-GĂłmez E
- Alessandri C
- Ali M
- Alim Al-Bari MA
- Aliwaini S
- Alizadeh J
- Almacellas E
- Almasan A
- Alonso A
- Alonso GD
- Altan-Bonnet N
- Altieri DC
- Alves da Costa C
- Alves S
- Alzaharna MM
- Amadio M
- Amantini C
- Amaral C
- Ambrosio S
- Amer AO
- Ammanathan V
- An Z
- Andersen SU
- Andrabi SA
- Andrade-Silva M
- Andres AM
- Angelini S
- Ann D
- Anozie UC
- Ansari MY
- Antas P
- Antebi A
- AntĂłn Z
- Anwar T
- Apetoh L
- Apostolova N
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- Araki Y
- Arasaki K
- Araya J
- AraĂșjo WL
- Arden C
- Arguelles S
- Arias E
- Arikkath J
- Arimoto H
- Ariosa AR
- Armstrong-James D
- Arnauné-Pelloquin L
- Aroca A
- Arroyo DS
- Arsov I
- Artero R
- Arévalo M-A
- Asaro DML
- Aschner M
- Ashrafizadeh M
- Ashur-Fabian O
- Atanasov AG
- Au AK
- Auberger P
- Auner HW
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- Autelli R
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- Aveic S
- Aveleira CA
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- Mysorekar IU
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- Silva-Pavez E
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- Simmonds RE
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- Simons M
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- Sluimer JC
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- Stalnecker CA
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- Stefan K
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- Steinkasserer A
- Stenmark H
- Sterneckert J
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- Strohecker AM
- Stupack DG
- Su H
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- Subauste CS
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- Sudhandiran G
- Sue CM
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- Sunahara KKS
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- Titorenko VI
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- Toivonen JM
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- Tomar D
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- Tong BC-K
- Tong C
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- Tooze SA
- Torgersen ML
- Torii S
- Torres-LĂłpez L
- Torriglia A
- Towers CG
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- Toyokuni S
- Trajkovic V
- Tramontano D
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- Travassos LH
- Trelford CB
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- Trougakos IP
- Tsao BP
- Tschan MP
- Tse H-F
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- Tsugawa H
- Tsvetkov AS
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- Tumtas Y
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- Turner BJ
- Tuxworth RI
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- van Wijk SJL
- Vandenberghe W
- Vanhorebeek I
- Vannier-Santos MA
- Vannini N
- Vanrell MC
- Vantaggiato C
- Varano G
- Varela-Nieto I
- Varga M
- Vasconcelos MH
- Vats S
- Vavvas DG
- Vega-Naredo I
- Vega-Rubin-de-Celis S
- Velasco G
- Vellai T
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- Waguri S
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- Wang B
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- Wang W
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- Wang X
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- Warnsmann V
- Watada H
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- Wehman AM
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- Wei L
- Wei T
- Wei Y
- WeiergrÀber OH
- Weihl CC
- Weindl G
- Weiskirchen R
- Wells A
- Wen RH
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- Weykopf B
- Wheatley SP
- Whitton JL
- Whitworth AJ
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- Wildenberg ME
- Wileman T
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- Wodrich H
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- Wollert T
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- Wong JH
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- Wu A-G
- Wu C
- Wu J
- Wu J
- Wu KK
- Wu M
- Wu S
- Wu S
- Wu S-Y
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- Wu WKK
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- Xavier RJ
- Xia H
- Xia L
- Xia Z
- Xiang G
- Xiang J
- Xiang M
- Xiang W
- Xiao B
- Xiao G
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- Xiao H-T
- Xiao J
- Xiao L
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- Xiao Y
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- Xilouri M
- Xu C
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- Yakhine-Diop SMS
- Yamaguchi M
- Yamaguchi O
- Yamamoto A
- Yamashina S
- Yan S
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- Yanagi Y
- Yang C
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- Yang W
- Yang WY
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- Yang Y
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- Yao H
- Yao S
- Yao X
- Yao Y-G
- Yao Y-M
- Yasui T
- Yazdankhah M
- Yen PM
- Yi C
- Yi-Ren Hong C-WH
- Yin X-M
- Yin Y
- Yin Z
- Yin Z
- Ying M
- Ying Z
- Yip CK
- Yiu SPT
- Yoo YH
- Yoshida K
- Yoshii SR
- Yoshimori T
- Yousefi B
- Yu B
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- Yu J
- Yu J
- Yu L
- Yu M-L
- Yu S-W
- Yu VC
- Yu WH
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- Yuan S-SF
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- Yuan Z
- Yue J
- Yue Z
- Yun J
- Yung RL
- Zacks DN
- Zaffagnini G
- Zambelli VO
- Zanella I
- Zang QS
- Zanivan S
- Zappavigna S
- Zaragoza P
- Zarbalis KS
- Zarebkohan A
- Zarrouk A
- Zeitlin SO
- Zeng J
- Zeng J-D
- Zhan L
- Zhang B
- Zhang DD
- Zhang H
- Zhang H
- Zhang H
- Zhang H
- Zhang H
- Zhang H
- Zhang H
- Zhang H-L
- Zhang J
- Zhang J
- Zhang J-P
- Zhang KYB
- Zhang L
- Zhang L
- Zhang L
- Zhang L
- Zhang LW
- Zhang M
- Zhang P
- Zhang S
- Zhang W
- Zhang X
- Zhang X
- Zhang X
- Zhang X
- Zhang X
- Zhang X-W
- Zhang XD
- Zhang Y
- Zhang Y
- Zhang Y
- Zhang Y
- Zhang Y
- Zhang Y-D
- Zhang Y-Y
- Zhang Z
- Zhang Z
- Zhang Z
- Zhang Z
- Zhang Z
- Zhang Z
- Zhao H
- Zhao L
- Zhao S
- Zhao T
- Zhao X-F
- Zhao Y
- Zhao Y
- Zhao Y
- Zhao Y
- Zheng G
- Zheng K
- Zheng L
- Zheng S
- Zheng X-L
- Zheng Y
- Zheng Z-G
- Zhivotovsky B
- Zhong Q
- Zhou A
- Zhou B
- Zhou C
- Zhou G
- Zhou H
- Zhou H
- Zhou H
- Zhou J
- Zhou J
- Zhou J
- Zhou J
- Zhou K
- Zhou R
- Zhou X-J
- Zhou Y
- Zhou Y
- Zhou Y
- Zhou Z
- Zhou Z-Y
- Zhu B
- Zhu C
- Zhu G-Q
- Zhu H
- Zhu H
- Zhu H
- Zhu W-G
- Zhu Y
- Zhu Y
- Zhuang H
- Zhuang X
- Zientara-Rytter K
- Zimmermann CM
- Ziviani E
- Zoladek T
- Zong W-X
- Zorov DB
- Zorzano A
- Zou W
- Zou Z
- Zou Z
- Zuryn S
- Zwerschke W
- Ălvarez ĂMC
- Ăvalos Y
- Ănal G
- ĂstĂŒn S
- ÄoliÄ M
- ÄokiÄ J
- Ćœerovnik E
- Publication venue
- 'Informa UK Limited'
- Publication date
- 01/01/2021
- Field of study
In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes. These guidelines are not meant to be a dogmatic set of rules, because the appropriateness of any assay largely depends on the question being asked and the system being used. Moreover, no individual assay is perfect for every situation, calling for the use of multiple techniques to properly monitor autophagy in each experimental setting. Finally, several core components of the autophagy machinery have been implicated in distinct autophagic processes (canonical and noncanonical autophagy), implying that genetic approaches to block autophagy should rely on targeting two or more autophagy-related genes that ideally participate in distinct steps of the pathway. Along similar lines, because multiple proteins involved in autophagy also regulate other cellular pathways including apoptosis, not all of them can be used as a specific marker for bona fide autophagic responses. Here, we critically discuss current methods of assessing autophagy and the information they can, or cannot, provide. Our ultimate goal is to encourage intellectual and technical innovation in the field
Molekulare und funktionale Analyse des Ephrin-A5-Gens der Maus.
- Author
- Publication venue
- Neuherberg : GSF-Forschungszentrum mbH
- Publication date
- 01/01/2000
- Field of study
Expression domains of murine ephrin-A5 in the pituitary and hypothalamus.
- Author
- Publication venue
- Publication date
- 01/01/2000
- Field of study
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