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Article ; Online: Gene of the month: the uroplakins.

Sivakumaar, Krithicck / Griffin, Jon / Schofield, Ella / Catto, James W F / Jubber, Ibrahim

2024 Volume 77, Issue 5, Page(s) 291–296

Abstract: Uroplakins are a family of membrane-spanning proteins highly specific to the urothelium. There are four uroplakin proteins in humans. These are encoded by the ... ...

Abstract	Uroplakins are a family of membrane-spanning proteins highly specific to the urothelium. There are four uroplakin proteins in humans. These are encoded by the following
MeSH term(s)	Humans ; Uroplakins/genetics ; Uroplakins/metabolism ; Membrane Proteins/genetics ; Urinary Bladder ; Urinary Bladder Neoplasms/genetics ; Urinary Bladder Neoplasms/pathology ; Urothelium/pathology
Chemical Substances	Uroplakins ; Membrane Proteins
Language	English
Publishing date	2024-04-18
Publishing country	England
Document type	Journal Article
ZDB-ID	80261-x
ISSN	1472-4146 ; 0021-9746
ISSN (online)	1472-4146
ISSN	0021-9746
DOI	10.1136/jcp-2024-209388
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Article ; Online: Gene of the month: GATA3.

Qiang, Zekai / Jubber, Ibrahim / Lloyd, Kirsty / Cumberbatch, Marcus / Griffin, Jon

Journal of clinical pathology

2023 Volume 76, Issue 12, Page(s) 793–797

Abstract: ... processes. GATA3 regulates gene expression through binding nucleosomal DNA and facilitating chromatin ...

Abstract	GATA binding protein 3 (GATA3) is a zinc-finger pioneer transcription factor involved in diverse processes. GATA3 regulates gene expression through binding nucleosomal DNA and facilitating chromatin remodelling. Post-translational modifications modulate its activity. During development, GATA3 plays a key role in cell differentiation. Mutations in
MeSH term(s)	Humans ; Female ; Breast/metabolism ; Urinary Bladder Neoplasms/genetics ; Mutation ; GATA3 Transcription Factor/genetics ; GATA3 Transcription Factor/metabolism ; Breast Neoplasms ; Biomarkers, Tumor/genetics
Chemical Substances	GATA3 Transcription Factor ; Biomarkers, Tumor ; GATA3 protein, human
Language	English
Publishing date	2023-09-19
Publishing country	England
Document type	Review ; Journal Article
ZDB-ID	80261-x
ISSN	1472-4146 ; 0021-9746
ISSN (online)	1472-4146
ISSN	0021-9746
DOI	10.1136/jcp-2023-209017
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Article ; Online: Gene of the month: NKX3.1.

Griffin, Jon / Chen, Yuqing / Catto, James W F / El-Khamisy, Sherif

Journal of clinical pathology

2022 Volume 75, Issue 6, Page(s) 361–364

Abstract: NKX3.1 is a multifaceted protein with roles in prostate development and protection from oxidative stress. Acting as a pioneer factor, NKX3.1 interacts with chromatin at enhancers to help integrate androgen regulated signalling. In prostate cancer, NKX3.1 ...

Abstract	NKX3.1 is a multifaceted protein with roles in prostate development and protection from oxidative stress. Acting as a pioneer factor, NKX3.1 interacts with chromatin at enhancers to help integrate androgen regulated signalling. In prostate cancer, NKX3.1 activity is frequently reduced through a combination of mutational and post-translational events. Owing to its specificity for prostate tissue, NKX3.1 has found use as an immunohistochemical marker in routine histopathology practice.
MeSH term(s)	Androgens/metabolism ; Homeodomain Proteins/genetics ; Humans ; Male ; Prostatic Neoplasms/pathology ; Transcription Factors/genetics
Chemical Substances	Androgens ; Homeodomain Proteins ; NKX3-1 protein, human ; Transcription Factors
Language	English
Publishing date	2022-01-07
Publishing country	England
Document type	Journal Article
ZDB-ID	80261-x
ISSN	1472-4146 ; 0021-9746
ISSN (online)	1472-4146
ISSN	0021-9746
DOI	10.1136/jclinpath-2021-208073
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Article ; Online: NaRnEA: An Information Theoretic Framework for Gene Set Analysis.

Griffin, Aaron T / Vlahos, Lukas J / Chiuzan, Codruta / Califano, Andrea

Entropy (Basel, Switzerland)

2023 Volume 25, Issue 3

Abstract: Gene sets are being increasingly leveraged to make high-level biological inferences ... from transcriptomic data; however, existing gene set analysis methods rely on overly conservative, heuristic ... approaches for quantifying the statistical significance of gene set enrichment. We created Nonparametric ...

Abstract	Gene sets are being increasingly leveraged to make high-level biological inferences from transcriptomic data; however, existing gene set analysis methods rely on overly conservative, heuristic approaches for quantifying the statistical significance of gene set enrichment. We created Nonparametric analytical-Rank-based Enrichment Analysis (NaRnEA) to facilitate accurate and robust gene set analysis with an optimal null model derived using the information theoretic Principle of Maximum Entropy. By measuring the differential activity of ~2500 transcriptional regulatory proteins based on the differential expression of each protein's transcriptional targets between primary tumors and normal tissue samples in three cohorts from The Cancer Genome Atlas (TCGA), we demonstrate that NaRnEA critically improves in two widely used gene set analysis methods: Gene Set Enrichment Analysis (GSEA) and analytical-Rank-based Enrichment Analysis (aREA). We show that the NaRnEA-inferred differential protein activity is significantly correlated with differential protein abundance inferred from independent, phenotype-matched mass spectrometry data in the Clinical Proteomic Tumor Analysis Consortium (CPTAC), confirming the statistical and biological accuracy of our approach. Additionally, our analysis crucially demonstrates that the sample-shuffling empirical null models leveraged by GSEA and aREA for gene set analysis are overly conservative, a shortcoming that is avoided by the newly developed Maximum Entropy analytical null model employed by NaRnEA.
Language	English
Publishing date	2023-03-21
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2014734-X
ISSN	1099-4300 ; 1099-4300
ISSN (online)	1099-4300
ISSN	1099-4300
DOI	10.3390/e25030542
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Article ; Online: Simplified homology-assisted CRISPR for gene editing in Drosophila.

G3 (Bethesda, Md.)

2023 Volume 14, Issue 2

Abstract: ... generates powerful tools to study gene regulation and function. We revised the homology-assisted CRISPR ...

Abstract	In vivo genome editing with clustered regularly interspaced short palindromic repeats (CRISPR)/Cas9 generates powerful tools to study gene regulation and function. We revised the homology-assisted CRISPR knock-in method to convert Drosophila GAL4 lines to LexA lines using a new universal knock-in donor strain. A balancer chromosome-linked donor strain with both body color (yellow) and eye red fluorescent protein (RFP) expression markers simplified the identification of LexA knock-in using light or fluorescence microscopy. A second balancer chromosome-linked donor strain readily converted the second chromosome-linked GAL4 lines regardless of target location in the cis-chromosome but showed limited success for the third chromosome-linked GAL4 lines. We observed a consistent and robust expression of the yellow transgene in progeny harboring a LexA knock-in at diverse genomic locations. Unexpectedly, the expression of the 3xP3-RFP transgene in the "dual transgene" cassette was significantly increased compared with that of the original single 3xP3-RFP transgene cassette in all tested genomic locations. Using this improved screening approach, we generated 16 novel LexA lines; tissue expression by the derived LexA and originating GAL4 lines was similar or indistinguishable. In collaboration with 2 secondary school classes, we also established a systematic workflow to generate a collection of LexA lines from frequently used GAL4 lines.
MeSH term(s)	Animals ; Gene Editing/methods ; Drosophila/genetics ; Transgenes ; Genome ; CRISPR-Cas Systems
Language	English
Publishing date	2023-12-07
Publishing country	England
Document type	Journal Article
ZDB-ID	2629978-1
ISSN	2160-1836 ; 2160-1836
ISSN (online)	2160-1836
ISSN	2160-1836
DOI	10.1093/g3journal/jkad277
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Article ; Online: Disruption of the gene regulatory programme in neurodevelopmental disorders.

Griffin, Aoife / Mahesh, Arun / Tiwari, Vijay K

Biochimica et biophysica acta. Gene regulatory mechanisms

2022 Volume 1865, Issue 7, Page(s) 194860

Abstract: ... that gene expression programs governing these events rely on the interplay between signalling molecules ... to highlight how recent advances in technologies have helped uncover and imitate the gene regulatory mechanisms ...

Abstract	Cortical development consists of a series of synchronised events, including fate transition of cortical progenitors, neuronal migration, specification and connectivity. It is becoming clear that gene expression programs governing these events rely on the interplay between signalling molecules, transcription factors and epigenetic mechanisms. When genetic or environmental factors disrupt expression of genes involved in important brain development processes, neurodevelopmental disorders can occur. This review aims to highlight how recent advances in technologies have helped uncover and imitate the gene regulatory mechanisms commonly disrupted in neurodevelopmental disorders.
MeSH term(s)	Epigenesis, Genetic ; Humans ; Neurodevelopmental Disorders/genetics ; Neurogenesis/genetics ; Transcription Factors/genetics
Chemical Substances	Transcription Factors
Language	English
Publishing date	2022-08-23
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	2918786-2
ISSN	1876-4320 ; 1874-9399
ISSN (online)	1876-4320
ISSN	1874-9399
DOI	10.1016/j.bbagrm.2022.194860
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Article: Study of Canine Distemper Virus Presence in Catalonia's Wild Carnivores through H Gene Amplification and Sequencing.

Huang, Junhao / Cortey, Martí / Darwich, Laila / Griffin, Jenna / Obón, Elena / Molina, Rafael / Martín, Margarita

Animals : an open access journal from MDPI

2024 Volume 14, Issue 3

Abstract: ... in Torreferrussa. RT-PCR and sequencing of the partial H gene were used to detect and analyse CDV in tissues ...

Abstract	Canine distemper virus (CDV) is recognised worldwide as an important pathogen in both domestic and wild carnivores. Few data are available on its impact and spread on the wildlife/wildlife-domestic animal-environment interface. This study, aimed at developing a conservation-oriented control strategy, analysed 89 sick or deceased animals from 2019 to 2023 at the Wildlife Rehabilitation Centre in Torreferrussa. RT-PCR and sequencing of the partial H gene were used to detect and analyse CDV in tissues. The total positive percentage was 20.22% (18/89), comprising 13 red foxes (44.8%), 4 European badgers (28.6%), and 1 American mink (4.5%), while 24 Eurasian otters tested negative. Phylogenetic analysis indicated that all of the CDV strains belong to the European lineage. Geographically distant individuals and different species shared the same viral strain, suggesting a strong capacity of CDV for interspecies and long-distance transmission. This calls for further research, particularly focusing on potential impacts of CDV on endangered carnivores.
Language	English
Publishing date	2024-01-29
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2606558-7
ISSN	2076-2615
ISSN	2076-2615
DOI	10.3390/ani14030436
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Article ; Online: Swine influenza A virus isolates containing the pandemic H1N1 origin matrix gene elicit greater disease in the murine model.

Curran, Shelly J / Griffin, Emily F / Ferreri, Lucas M / Kyriakis, Constantinos S / Howerth, Elizabeth W / Perez, Daniel R / Tompkins, S Mark

Microbiology spectrum

2024 Volume 12, Issue 3, Page(s) e0338623

Abstract: ... gene segment constellation, the triple reassortment internal gene (TRIG) cassette. In 2009, the H1N1 ... contributed the matrix gene (pdmM) to the swFLUAVs circulating in the pig population, which replaced ... the classical swine matrix gene (swM) found in the TRIG cassette, suggesting the pdmM has a fitness benefit ...

Abstract	Since the 1990s, endemic North American swine influenza A viruses (swFLUAVs) contained an internal gene segment constellation, the triple reassortment internal gene (TRIG) cassette. In 2009, the H1N1 pandemic (pdmH1N1) virus spilled back into swine but did not become endemic. However, the pdmH1N1 contributed the matrix gene (pdmM) to the swFLUAVs circulating in the pig population, which replaced the classical swine matrix gene (swM) found in the TRIG cassette, suggesting the pdmM has a fitness benefit. Others have shown that swFLUAVs containing the pdmM have greater transmission efficiency compared to viruses containing the swM gene segment. We hypothesized that the matrix (M) gene could also affect disease and utilized two infection models, resistant BALB/c and susceptible DBA/2 mice, to assess pathogenicity. We infected BALB/c and DBA/2 mice with H1 and H3 swFLUAVs containing the swM or pdmM and measured lung virus titers, morbidity, mortality, and lung histopathology. H1 influenza strains containing the pdmM gene caused greater morbidity and mortality in resistant and susceptible murine strains, while H3 swFLUAVs caused no clinical disease. However, both H1 and H3 swFLUAVs containing the pdmM replicated to higher viral titers in the lungs and pdmM containing H1 viruses induced greater histological changes compared to swM H1 viruses. While the surface glycoproteins and other gene segments may contribute to swFLUAV pathogenicity in mice, these data suggest that the origin of the matrix gene also contributes to pathogenicity of swFLUAV in mice, although we must be cautious in translating these conclusions to their natural host, swine. Importance: The 2009 pandemic H1N1 virus rapidly spilled back into North American swine, reassorting with the already genetically diverse swFLUAVs. Notably, the M gene segment quickly replaced the classical M gene segment, suggesting a fitness benefit. Here, using two murine models of infection, we demonstrate that swFLUAV isolates containing the pandemic H1N1 origin M gene caused increased disease compared to isolates containing the classical swine M gene. These results suggest that, in addition to other influenza virus gene segments, the swFLUAV M gene segment contributes to pathogenesis in mammals.
MeSH term(s)	Swine ; Mice ; Animals ; Humans ; Influenza, Human ; Influenza A Virus, H1N1 Subtype/genetics ; Disease Models, Animal ; Mice, Inbred DBA ; Orthomyxoviridae Infections/pathology ; Swine Diseases ; Mammals
Language	English
Publishing date	2024-02-01
Publishing country	United States
Document type	Journal Article
ZDB-ID	2807133-5
ISSN	2165-0497 ; 2165-0497
ISSN (online)	2165-0497
ISSN	2165-0497
DOI	10.1128/spectrum.03386-23
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Article ; Online: Gene therapy with bidridistrogene xeboparvovec for limb-girdle muscular dystrophy type 2E/R4: phase 1/2 trial results.

Mendell, Jerry R / Pozsgai, Eric R / Lewis, Sarah / Griffin, Danielle A / Lowes, Linda P / Alfano, Lindsay N / Lehman, Kelly J / Church, Kathleen / Reash, Natalie F / Iammarino, Megan A / Sabo, Brenna / Potter, Rachael / Neuhaus, Sarah / Li, Xiaoxi / Stevenson, Herb / Rodino-Klapac, Louise R

Nature medicine

2024 Volume 30, Issue 1, Page(s) 199–206

Abstract: Limb-girdle muscular dystrophy 2E/R4 is caused by mutations in the β-sarcoglycan (SGCB) gene ... leading to SGCB deficiency and consequent muscle loss. We developed a gene therapy approach based ... xeboparvovec, an adeno-associated virus-based gene therapy containing a codon-optimized, full-length human SGCB ...

Abstract	Limb-girdle muscular dystrophy 2E/R4 is caused by mutations in the β-sarcoglycan (SGCB) gene, leading to SGCB deficiency and consequent muscle loss. We developed a gene therapy approach based on functional replacement of the deficient SCB protein. Here we report interim results from a first-in-human, open-label, nonrandomized, phase 1/2 trial evaluating the safety and efficacy of bidridistrogene xeboparvovec, an adeno-associated virus-based gene therapy containing a codon-optimized, full-length human SGCB transgene. Patients aged 4-15 years with confirmed SGCB mutations at both alleles received one intravenous infusion of either 1.85 × 10
MeSH term(s)	Humans ; Muscular Dystrophies, Limb-Girdle/genetics ; Muscular Dystrophies, Limb-Girdle/metabolism ; Muscular Dystrophies, Limb-Girdle/therapy ; Sarcoglycanopathies/genetics ; Sarcoglycanopathies/metabolism ; Sarcoglycanopathies/therapy ; Muscle, Skeletal/metabolism ; Genetic Therapy/adverse effects ; Genetic Therapy/methods
Language	English
Publishing date	2024-01-04
Publishing country	United States
Document type	Clinical Trial, Phase II ; Clinical Trial, Phase I ; Journal Article
ZDB-ID	1220066-9
ISSN	1546-170X ; 1078-8956
ISSN (online)	1546-170X
ISSN	1078-8956
DOI	10.1038/s41591-023-02730-9
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Zs.A 4212: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 39: Show issues

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Article ; Online: RORβ modulates a gene program that is protective against articular cartilage damage.

Chang, Mi Ra / Griffin, Patrick R

PloS one

2022 Volume 17, Issue 10, Page(s) e0268663

Abstract: ... in cultured cells results in alteration of a gene program that is supportive of chondrogenesis and is protective ...

Abstract	Osteoarthritis (OA) is the most prevalent chronic joint disease which increases in frequency with age eventually impacting most people over the age of 65. OA is the leading cause of disability and impaired mobility, yet the pathogenesis of OA remains unclear. Treatments have focused mainly on pain relief and reducing joint swelling. Currently there are no effective treatments to slow the progression of the disease and to prevent irreversible loss of cartilage. Here we demonstrate that stable expression of RORβ in cultured cells results in alteration of a gene program that is supportive of chondrogenesis and is protective against development of OA. Specifically, we determined that RORβ alters the ratio of expression of the FGF receptors FGFR1 (associated with cartilage destruction) and FGFR3 (associated with cartilage protection). Additionally, ERK1/2-MAPK signaling was suppressed and AKT signaling was enhanced. These results suggest a critical role for RORβ in chondrogenesis and suggest that identification of mechanisms that control the expression of RORβ in chondrocytes could lead to the development of disease modifying therapies for the treatment of OA.
MeSH term(s)	Cartilage, Articular/pathology ; Chondrocytes/metabolism ; Chondrogenesis/genetics ; Humans ; Osteoarthritis/genetics ; Osteoarthritis/prevention & control ; Proto-Oncogene Proteins c-akt/genetics ; Proto-Oncogene Proteins c-akt/metabolism
Chemical Substances	Proto-Oncogene Proteins c-akt (EC 2.7.11.1)
Language	English
Publishing date	2022-10-13
Publishing country	United States
Document type	Journal Article
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0268663
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