Jonathan M. Locke

1.5k total citations · 1 hit paper
22 papers, 798 citations indexed

About

Jonathan M. Locke is a scholar working on Surgery, Molecular Biology and Genetics. According to data from OpenAlex, Jonathan M. Locke has authored 22 papers receiving a total of 798 indexed citations (citations by other indexed papers that have themselves been cited), including 13 papers in Surgery, 10 papers in Molecular Biology and 7 papers in Genetics. Recurrent topics in Jonathan M. Locke's work include Pancreatic function and diabetes (13 papers), MicroRNA in disease regulation (5 papers) and Diabetes and associated disorders (5 papers). Jonathan M. Locke is often cited by papers focused on Pancreatic function and diabetes (13 papers), MicroRNA in disease regulation (5 papers) and Diabetes and associated disorders (5 papers). Jonathan M. Locke collaborates with scholars based in United Kingdom, United States and Finland. Jonathan M. Locke's co-authors include Lorna W. Harries, Guy A. Rutter, Andrew R. Wood, Michael N. Weedon, Gabriela da Silva Xavier, Sian Ellard, Andrew T. Hattersley, Seth A. Sharp, Helen R. Dawe and Robin N. Beaumont and has published in prestigious journals such as The Journal of Clinical Endocrinology & Metabolism, Diabetes Care and Diabetes.

In The Last Decade

Jonathan M. Locke

22 papers receiving 796 citations

Hit Papers

align trajectories

What are hit papers?

Hit papers significantly outperform the citation benchmark for their cohort. A paper qualifies if it has ≥500 total citations, achieves ≥1.5× the top-1% citation threshold for papers in the same subfield and year (this is the minimum needed to enter the top 1%, not the average within it), or reaches the top citation threshold in at least one of its specific research topics.

Development and Standardization of an Improved Type 1 Diabetes Genetic Risk Score for Use in Newborn Screening and Incident Diagnosis

2019 206 citations Seth A. Sharp, Stephen S. Rich et al. Diabetes Care profile →

Peers

Countries citing papers authored by Jonathan M. Locke

Since Specialization

Citations

This map shows the geographic impact of Jonathan M. Locke's research. It shows the number of citations coming from papers published by authors working in each country. You can also color the map by specialization and compare the number of citations received by Jonathan M. Locke with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Jonathan M. Locke more than expected).

Fields of papers citing papers by Jonathan M. Locke

Since Specialization

Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by Jonathan M. Locke. Nodes represent research fields, and links connect fields that are likely to share authors. Colored nodes show fields that tend to cite the papers produced by Jonathan M. Locke. The network helps show where Jonathan M. Locke may publish in the future.

Co-authorship network of co-authors of Jonathan M. Locke

This figure shows the co-authorship network connecting the top 25 collaborators of Jonathan M. Locke. A scholar is included among the top collaborators of Jonathan M. Locke based on the total number of citations received by their joint publications. Widths of edges represent the number of papers authors have co-authored together. Node borders signify the number of papers an author published with Jonathan M. Locke. Jonathan M. Locke is excluded from the visualization to improve readability, since they are connected to all nodes in the network.

All Works

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20 of 20 papers shown

#	Work	Indexed citations
1	Insights into the genetics of menopausal vasomotor symptoms: genome-wide analyses of routinely-collected primary care health records 2023 ·BMC Medical Genomics ·Katherine S. Ruth, Robin N. Beaumont, Jonathan M. Locke, Jessica Tyrrell, Carolyn Crandall, (unknown), Timothy M. Frayling, Julia Prague, Kashyap Patel, Andrew R. Wood, Michael N. Weedon, Anna Murray	4
2	Detection of enterovirus RNA in peripheral blood mononuclear cells correlates with the presence of the predisposing allele of the type 1 diabetes risk gene IFIH1 and with disease stage 2022 ·Diabetologia ·Amir‐Babak Sioofy‐Khojine, Sarah J. Richardson, Jonathan M. Locke, Sami Oikarinen, Noora Nurminen, Antti‐Pekka Laine, Kate Downes, Johanna Lempainen, John A. Todd, Riitta Veijola, Jorma Ilonen, Mikael Knip, Noel G. Morgan, Heikki Hyöty, Mark Peakman, Martin Eichmann	9
3	Loss of MANF Causes Childhood-Onset Syndromic Diabetes Due to Increased Endoplasmic Reticulum Stress 2021 ·Diabetes ·Hossam Montaser, Kashyap Patel, Diego Balboa, Hazem Ibrahim, Väinö Lithovius, Anna Näätänen, Vikash Chandra, Korcan Demir, Sezer Acar, Tawfeg Ben‐Omran, Kevin Colclough, Jonathan M. Locke, Matthew N. Wakeling, Maria Lindahl, Andrew T. Hattersley, Jonna Saarimäki‐Vire, Timo Otonkoski	46
4	Development and Standardization of an Improved Type 1 Diabetes Genetic Risk Score for Use in Newborn Screening and Incident Diagnosis breakdown → 2019 ·Diabetes Care ·Seth A. Sharp, Stephen S. Rich, Andrew R. Wood, Samuel E. Jones, Robin N. Beaumont, Jamie Harrison, Darius Schneider, Jonathan M. Locke, Jessica Tyrrell, Michael N. Weedon, William Hagopian, Richard A. Oram	206
5	The Common HNF1A Variant I27L Is a Modifier of Age at Diabetes Diagnosis in Individuals With HNF1A-MODY 2018 ·Diabetes ·Jonathan M. Locke, Cécile Saint‐Martin, Thomas W. Laver, Kashyap Patel, Andrew R. Wood, Seth A. Sharp, Sian Ellard, Christine Bellanné‐Chantelot, Andrew T. Hattersley, Lorna W. Harries, Michael N. Weedon	19
6	Functional characterisation of ADIPOQ variants using individuals recruited by genotype 2016 ·Molecular and Cellular Endocrinology ·Benjamin P. Lee, (unknown), Jonathan M. Locke, Laura McCulloch, Bridget Knight, Hanieh Yaghootkar, Giles O. Cory, Katarina Kos, Timothy M. Frayling, Lorna W. Harries	8
7	MAOA expression predicts vulnerability for alcohol use 2015 ·Molecular Psychiatry ·(unknown), (unknown), (unknown), Richard S. Lee, Jonathan M. Locke, C A Helms, (unknown), Gary S. Wand, Sara R. Jones, Kathleen A. Grant, Betsy Ferguson	32
8	A cautionary tale: the non-causal association between type 2 diabetes risk SNP, rs7756992, and levels of non-coding RNA, CDKAL1-v1 2015 ·Diabetologia ·Jonathan M. Locke, Fan‐Yan Wei, Kazuhito Tomizawa, Michael N. Weedon, Lorna W. Harries	16
9	Role of microRNAs in the age-associated decline of pancreatic beta cell function in rat islets 2015 ·Diabetologia ·(unknown), Claudiane Guay, Ana Claudia Marques, Florent Allagnat, Jonathan M. Locke, Lorna W. Harries, Guy A. Rutter, Romano Regazzi	37
10	Targeted Allelic Expression Profiling in Human Islets Identifies cis-Regulatory Effects for Multiple Variants Identified by Type 2 Diabetes Genome-Wide Association Studies 2014 ·Diabetes ·Jonathan M. Locke, Gerald Hysenaj, Andrew R. Wood, Michael N. Weedon, Lorna W. Harries	30
11	Increased expression of miR-187 in human islets from individuals with type 2 diabetes is associated with reduced glucose-stimulated insulin secretion 2013 ·Diabetologia ·Jonathan M. Locke, Gabriela da Silva Xavier, Helen R. Dawe, Guy A. Rutter, Lorna W. Harries	90
12	The splice site variant rs11078928 may be associated with a genotype-dependent alteration in expression of GSDMB transcripts 2013 ·BMC Genomics ·(unknown), Jonathan M. Locke, Andrew R. Wood, Marcus A. Tuke, Dorota Pasko, Anna Murray, Timothy M. Frayling, Lorna W. Harries	23
13	Expression Profiling of Type 2 Diabetes Susceptibility Genes in the Pancreatic Islets, Adipose Tissue and Liver of Obese Mice 2013 ·Experimental and Clinical Endocrinology & Diabetes ·(unknown), Jonathan M. Locke, (unknown), Anna Murray, Janet Brown, Lorna W. Harries	4
14	A rare SNP in pre-miR-34a is associated with increased levels of miR-34a in pancreatic beta cells 2013 ·Acta Diabetologica ·Jonathan M. Locke, Hana Lango Allen, Lorna W. Harries	26
15	Oxidative Metabolism Genes Are Not Responsive to Oxidative Stress in Rodent Beta Cell Lines 2012 ·Experimental Diabetes Research ·(unknown), Karen A. Johnstone, Anna Murray, Jonathan M. Locke, Lorna W. Harries	4
16	An alternative polyadenylation signal in TCF7L2 generates isoforms that inhibit T cell factor/lymphoid-enhancer factor (TCF/LEF)-dependent target genes 2011 ·Diabetologia ·Jonathan M. Locke, Gabriela da Silva Xavier, Guy A. Rutter, Lorna W. Harries	35
17	Genome-Wide Homozygosity Analysis Reveals HADH Mutations as a Common Cause of Diazoxide-Responsive Hyperinsulinemic-Hypoglycemia in Consanguineous Pedigrees 2011 ·The Journal of Clinical Endocrinology & Metabolism ·Sarah E. Flanagan, Ann‐Marie Patch, Jonathan M. Locke, Teoman Akçay, Enver Şimşek, (unknown), (unknown), Meena Desai, Ritika R. Kapoor, Khalid Hussain, Sian Ellard	41
18	Recessive mutations in the INS gene; a novel common cause of permanent neonatal diabetes in consanguineous pedigrees 2008 ·Queensland's institutional digital repository (The University of Queensland) ·(unknown), Jonathan M. Locke, Sarah E. Flanagan, Ann‐Marie Patch, Lorna W. Harries, Sian Ellard, Andrew T. Hattersley	2
19	Persistent Hyperinsulinemic Hypoglycemia and Maturity-Onset Diabetes of the Young Due to Heterozygous HNF4A Mutations 2008 ·Diabetes ·Ritika R. Kapoor, Jonathan M. Locke, Kevin Colclough, J K Wales, Jennifer Conn, Andrew T. Hattersley, Sian Ellard, Khalid Hussain	97
20	The Diabetic Phenotype in HNF4A Mutation Carriers Is Moderated By the Expression of HNF4A Isoforms From the P1 Promoter During Fetal Development 2008 ·Diabetes ·Lorna W. Harries, Jonathan M. Locke, Beverley M. Shields, Neil A. Hanley, Karen Piper Hanley, Anna Steele, Pål R. Njølstad, Sian Ellard, Andrew T. Hattersley	57

Rankless uses publication and citation data sourced from OpenAlex, an open and comprehensive bibliographic database. While OpenAlex provides broad and valuable coverage of the global research landscape, it—like all bibliographic datasets—has inherent limitations. These include incomplete records, variations in author disambiguation, differences in journal indexing, and delays in data updates. As a result, some metrics and network relationships displayed in Rankless may not fully capture the entirety of a scholar's output or impact.

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