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Grant Stewart @GS_Lab_Bham

The Stewart lab has a long-standing interest in studying rare human diseases associated with defective DNA repair and/or abnormal DNA replication.

Joined March 2020
  • Tweets 919
  • Following 417
  • Followers 1,670
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Grant Stewart@GS_Lab_Bham
19 Dec 2025
Awesome collaboration with @SPJacksonGroup, Chris Carney and Soren Hough, understanding how inherited mutations in the MEAE E3 ubiquitin ligase causes disease by compromising HR-dependent replication fork protection/restart. link.springer.com/article/10…

Loss of CTLH component MAEA impairs DNA repair and replication and leads to developmental delay

EMBO Molecular Medicine - Ubiquitin E3 ligases play crucial roles in the DNA damage response (DDR) by modulating the turnover, localization, activation, and interactions of DDR and DNA replication...

link.springer.com
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Peter Ly@PeterLyLab
May 19
Excited to share our latest paper, out today @CellCellPress. We found that large pieces of the human genome can transfer between cells upon direct contact, endowing recipient cells with heritable phenotypic changes. (1/7) cell.com/cell/fulltext/S0092…
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Finally our collaborative paper on inherited mutations in the actin nulceating factor, DIAPH1, spear-headed by the Houlden lab, @RMaroofian, Valentina Galassi Deforie, @StephanieEfthy1 and Peter Arkwright, is out in Genetics in Medicine. gimjournal.org/article/S1098…

Recessive loss of DIAPH1 function causes a progressive neurodevelopmental syndrome with variable...

Biallelic DIAPH1 pathogenic variants cause a neurodevelopmental syndrome occasionally associated with immunodeficiency. This study aims to define the clinical and immunological spectrum of DIAPH1-r...

gimjournal.org
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Interested in inherited chromosomal instability syndromes and DNA repair? We are looking for an enthusiastic person to join the Stewart lab at the University of Birmingham as a senior technician. If you are interested, please have a look at the job advert: jobs.ac.uk/job/DPH515/senior…
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Great work by the Kitagawa lab about DONSON regulating centrosome duplication is finally out in Nature Comms nature.com/articles/s41467-0…
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Great paper by the Vaziri lab about the role of RNF25 regulating the DDR independently of its E3 ligase activity! nature.com/articles/s41467-0…

The RING finger E3 ligase RNF25 protects DNA replication forks independently of its canonical roles...

Nature Communications - DNA replication stress is a driver of genome instability. Here, the authors identify a role of the E3 ligase RNF25 in promoting replication stress tolerance....

nature.com
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Grant Stewart retweeted
altmeyerlab@altmeyerlab
31 Jul 2025
New work from the lab: Identification of CNOT1-CCR4-NOT as a suppressor of 53BP1-p53-p21 signaling @CellReports. Congratulations to first author Antonio Galarreta and to all co-authors. cell.com/cell-reports/fullte…. #Microscopy #RNAiScreen #Condensates
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Suyang Zhang@Zhang_Suyang
7 Jul 2025
A transcription balance required for genome stability 🧬⚖️ Our work on RNA Pol II transcription speed control by the DNA helicase RECQL5 and the transcription-coupled DNA repair complex is now on ⁦⁦@NatureSMB⁩ #CryoEM #transcription nature.com/articles/s41594-0…

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Garcia lab@PgGarcialab
1 Jul 2025
Delighted to announce that our paper showing the generation of iPSc from a MDS patient & how CEBPA drives disease progression is finally out in Nature Comms! A big thanks to everybody involved & the great collaborators that have made it possible! nature.com/articles/s41467-0…

A heterozygous CEBPA mutation disrupting the bZIP domain in a RUNX1 and SRSF2 mutational background...

Nature Communications - In Myeloiddysplastic syndromes, CEBPA mutations are linked to disease progression and AML. Here, the authors use somatic reprogramming and genome editing to generate...

nature.com
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Molecular Cell@MolecularCell
26 Jun 2025
Online Now: The DNA replication checkpoint prevents PCNA/RFC depletion to protect forks from HLTF-induced collapse in human cells dlvr.it/TLZtS1
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Molecular Cell@MolecularCell
26 Jun 2025
Online Now: The DNA replication checkpoint limits Okazaki fragment accumulation to protect and restart stalled forks dlvr.it/TLZkmH
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andre nussenzweig lab@nussenza
25 Jun 2025
Cytarabine has been the mainstay for AML treatment. This chemotherapy can lead to problems with movement and balance. Here we explain this neurotoxic side effect: nature.com/articles/s41586-0…. Work led by Jia-Cheng Liu, Donpgeng Wang, Elsa Callen and many terrific collaborators!

Mechanism of cytarabine-induced neurotoxicity

Nature - Certain antimetabolites used to treat cancer are more neurotoxic than others, and it is now shown that this is due to their greater tendency to generate DNA double-stranded breaks, whereas...

nature.com
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Grant Stewart retweeted
The Blackford Lab@DrAndyBlackford
29 May 2025
We’re #hiring, please share! A fully funded #postdoc position is available in my lab to work on DNA damage response mechanisms. Please get in touch with your CV if you are interested, closing date: 27th June 2025. More details here: candidate.hr-manager.net/App…

Postdoctoral Research Associate in the Blackford Group

candidate.hr-manager.net
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Awesome paper from @SPJacksonGroup and @FrogWalterLab about USP37 and TRAIP regulating the replication response to topoisomerase inhibitors. Glad to be a part of it. nature.com/articles/s41467-0…

USP37 prevents premature disassembly of stressed replisomes by TRAIP

Nature Communications - The replicative helicase CMG is targeted for removal or proteolysis by the E3 ubiquitin ligase TRAIP. This study describes how the de-ubiquitylating enzyme USP37 protects...

nature.com
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Ivan Ahel Lab@IvanAhelLab
24 May 2025
Our new paper describing the RNF114 protein as a reader of dual hydrid modification composed of ADP-ribose and ubiquitin (ADPr-Ub) we discovered a few years ago (collaboration with the lab of Gerbrand van der Heden van Noort) biorxiv.org/content/10.1101/…

Identification of RNF114 as ADPr-Ub reader through non-hydrolysable ubiquitinated ADP-ribose

Crosstalk between the post-translational modification processes ubiquitination and ADP-ribosylation occurs in DNA-damage and immune-responses, in addition the physical linkage of ADP-ribose and...

biorxiv.org
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Proud to present our work identifying a role for DIAPH1 and gamma-actin in regulating DSB repair and how defects in this pathway give rise to human disease. Big thanks to everyone involved, especially Beth Woodward, Sudipta Lahiri and Anoop Chauhan. nature.com/articles/s41467-0…

Inherited deficiency of DIAPH1 identifies a DNA double strand break repair pathway regulated by...

Nature Communications - DNA double strand break repair pathways ensure genome stability and prevent disease. Here the authors show that the actin nucleating factor DIAPH1 and γ-actin promote...

nature.com
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Great collaborative study just out in Nature Communications about RNF168 regulation by PIN1. nature.com/articles/s41467-0…

PIN1-SUMO2/3 motif suppresses excessive RNF168 chromatin accumulation and ubiquitin signaling to...

Nature Communications - The ubiquitin ligase, RNF168, promotes DNA break repair but must be regulated to prevent run-away ubiquitin signaling. Here, the authors identify a three-step...

nature.com
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Grant Stewart retweeted
Cortés Lab@CortesLab
14 Apr 2021
Finally out! Congrats! @AndHR11 @SJimenoGonzalez @pmmargar @JoseT86910859 J. Lieberman and G. Millán Hope we contribute to the idea of supercoiling as a key regulator of genome metabolism, and not just a side-product of DNA transactions. More to come ... cell.com/cell-reports/fullte…

Topoisomerase IIα represses transcription by enforcing promoter-proximal pausing

Herrero-Ruiz et al. analyze the function of DNA topoisomerase II in transcriptional regulation. The results reveal that TOP2A activity favors promoter-proximal pausing of RNA polymerase II and...

cell.com
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Whilst it is not related to DNA repair or replication, an interesting study I was peripherally involved in is out now @JExpMed. Dominant mutations in ITPR3 cause combined immunodeficiency in humans. Congrats to Alexandra Kreins, the lead PI of this study. rupress.org/jem/article/222/…

Dominant negative variants in ITPR3 impair T cell Ca2 dynamics causing combined immunodeficiency

Dominant negative variants in ITPR3, encoding a subunit of the IP3 receptor, cause Ca2 channel leakiness resulting in ER store depletion and impaired T ce

rupress.org
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Grant Stewart retweeted
Rebecca Jones@RebeccaMJones4
15 Nov 2024
PhD position available in the Jones lab! warwick.ac.uk/fac/cross_fac/… @MIBTP_BBSRC programme. Understanding how DNA replication and the nuclear membrane deteriorate with age. With @ZitaBalklava @AstonUniversity Application deadline 16th Jan 2025
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