Nature Search

Development of a targeted BioPROTAC degrader selective for misfolded SOD1

Conventional PROTACs have limited capacity for misfolded proteins. Here, authors develop a BioPROTAC containing an scFv specifically targeting misfolded SOD1, fused to an E3 ligase, and demonstrate a strategy for reducing misfolded SOD1 accumulation.

Christen G. Chisholm
Rachael Bartlett
Justin J. Yerbury
ResearchOpen Access10 Nov 2025
Nature Communications

Volume: 16, P: 1-16
Upper Limit to the 11.4 m Flux of Saturn using VLBI

S. D. SHAWHAN
T. A. CLARK
J. P. BASART
Correspondence28 May 1973
Nature Physical Science

Volume: 243, P: 65-66
CCNF mutations in amyotrophic lateral sclerosis and frontotemporal dementia

Ian Blair and colleagues use genome-wide linkage analysis and whole exome sequencing to identify mutations in the CCNF gene in large cohorts of amyotrophic lateral sclerosis and frontotemporal dementia patients. In addition to validating the mutations in international cohorts, the authors also show that mutant CCNFgene product affects ubiquitination and protein degradation in cultured cells.

Kelly L. Williams
Simon Topp
Ian P. Blair
ResearchOpen Access15 Apr 2016
Nature Communications

Volume: 7, P: 1-8
p62 overexpression induces TDP-43 cytoplasmic mislocalisation, aggregation and cleavage and neuronal death

A. D. Foster
L. L. Flynn
S. L. Rea
ResearchOpen Access01 Jun 2021
Scientific Reports

Volume: 11, P: 1-16
Dynamic interplay between H-current and M-current controls motoneuron hyperexcitability in amyotrophic lateral sclerosis

Yossi Buskila
Orsolya Kékesi
Lezanne Ooi
ResearchOpen Access05 Apr 2019
Cell Death & Disease

Volume: 10, P: 1-13
The cysteine-reactive small molecule ebselen facilitates effective SOD1 maturation

Mutations in superoxide dismutase-1 (SOD1) cause amyotrophic lateral sclerosis (ALS). Here the authors present the SOD1 crystal structure bound to the small cysteine-reactive molecule ebselen and show that ebselen is a chaperone for SOD1.

Michael J. Capper
Gareth S. A. Wright
S. Samar Hasnain
ResearchOpen Access27 Apr 2018
Nature Communications

Volume: 9, P: 1-9
CuATSM improves motor function and extends survival but is not tolerated at a high dose in SOD1^G93A mice with a C57BL/6 background

Jeremy S. Lum
Mikayla L. Brown
Justin J. Yerbury
ResearchOpen Access29 Sept 2021
Scientific Reports

Volume: 11, P: 1-12
Protein disulphide isomerase (PDI) is protective against amyotrophic lateral sclerosis (ALS)-related mutant Fused in Sarcoma (FUS) in in vitro models

S. Parakh
E. R. Perri
J. D. Atkin
ResearchOpen Access02 Sept 2021
Scientific Reports

Volume: 11, P: 1-14
Rapid flow cytometric measurement of protein inclusions and nuclear trafficking

D. R. Whiten
R. San Gil
M. R. Wilson
ResearchOpen Access12 Aug 2016
Scientific Reports

Volume: 6, P: 1-9
Glutathionylation potentiates benign superoxide dismutase 1 variants to the toxic forms associated with amyotrophic lateral sclerosis

Luke McAlary
Justin J. Yerbury
J. Andrew Aquilina
ResearchOpen Access20 Nov 2013
Scientific Reports

Volume: 3, P: 1-6
High-content analysis of proteostasis capacity in cellular models of amyotrophic lateral sclerosis (ALS)

Isabella A. Lambert-Smith
Victoria K. Shephard
Darren N. Saunders
ResearchOpen Access15 Jun 2024
Scientific Reports

Volume: 14, P: 1-11
Tryptophan 32-mediated SOD1 aggregation is attenuated by pyrimidine-like compounds in living cells

Edward Pokrishevsky
Luke McAlary
Neil R. Cashman
ResearchOpen Access22 Oct 2018
Scientific Reports

Volume: 8, P: 1-12
Distinct partitioning of ALS associated TDP-43, FUS and SOD1 mutants into cellular inclusions

Natalie E. Farrawell
Isabella A. Lambert-Smith
Justin J. Yerbury
ResearchOpen Access21 Aug 2015
Scientific Reports

Volume: 5, P: 1-14
How we can make academia more disability inclusive

The low representation of academics with disabilities is a longstanding problem on which progress has been slow. Drawing on my research on disability-related barriers and my experiences of disability, I make six practical suggestions for how academic staff and people with disabilities can help make academia more disability inclusive.

Jonathan M. Levitt
Comments & Opinion15 Sept 2022
Nature Human Behaviour

Volume: 6, P: 1324-1326

Search

Development of a targeted BioPROTAC degrader selective for misfolded SOD1

Upper Limit to the 11.4 m Flux of Saturn using VLBI

CCNF mutations in amyotrophic lateral sclerosis and frontotemporal dementia

p62 overexpression induces TDP-43 cytoplasmic mislocalisation, aggregation and cleavage and neuronal death

Dynamic interplay between H-current and M-current controls motoneuron hyperexcitability in amyotrophic lateral sclerosis

The cysteine-reactive small molecule ebselen facilitates effective SOD1 maturation

CuATSM improves motor function and extends survival but is not tolerated at a high dose in SOD1^G93A mice with a C57BL/6 background

Protein disulphide isomerase (PDI) is protective against amyotrophic lateral sclerosis (ALS)-related mutant Fused in Sarcoma (FUS) in in vitro models

Rapid flow cytometric measurement of protein inclusions and nuclear trafficking

Glutathionylation potentiates benign superoxide dismutase 1 variants to the toxic forms associated with amyotrophic lateral sclerosis

High-content analysis of proteostasis capacity in cellular models of amyotrophic lateral sclerosis (ALS)

Tryptophan 32-mediated SOD1 aggregation is attenuated by pyrimidine-like compounds in living cells

Distinct partitioning of ALS associated TDP-43, FUS and SOD1 mutants into cellular inclusions

How we can make academia more disability inclusive

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