Mitogen-activated protein kinase phosphatase-1: function and regulation in bone and related tissues

Broome, David T.; Datta, Nabanita S.

doi:10.3109/03008207.2015.1125480

Cited by 12 publications

(10 citation statements)

References 141 publications

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“…rs2521349 resides in an intron of MAP2K6 on chromosome 17. MAP2K6 is an essential component of the p38 MAP kinase mediated signal transduction pathway, involved in various cellular processes in bone, muscle, fat tissue homeostasis and differentiation5. The MAPK signalling pathway has been closely associated with osteoblast differentiation6, chondrocyte apoptosis and necrosis7, and reported to be differentially expressed in osteoarthritis synovial tissue samples6–12.…”

Section: Resultsmentioning

confidence: 99%

Genome-wide analyses using UK Biobank data provide insights into the genetic architecture of osteoarthritis

et al. 2018

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Section: Resultsmentioning

confidence: 99%

Genome-wide analyses using UK Biobank data provide insights into the genetic architecture of osteoarthritis

et al. 2018

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“…rs2521349 resides in an intron of MAP2K6 on chromosome 17. MAP2K6 is an essential component of the p38 MAP kinase mediated signal transduction pathway, involved in various cellular processes in bone, muscle, fat tissue homeostasis and differentiation 27 . The MAPK signalling pathway has been closely associated with osteoblast differentiation, chondrocyte apoptosis and necrosis, and reported to be differentially expressed in OA synovial tissue samples [28][29][30][31][32][33][34][35][36][37][38] .…”

Section: Identification Of Novel Oa Locimentioning

confidence: 99%

The genetic architecture of osteoarthritis: insights from UK Biobank

Zengini

Hatzikotoulas

Tachmazidou

et al. 2017

Preprint

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Osteoarthritis is a common complex disease with huge public health burden. Here we perform a genome-wide association study for osteoarthritis using data across 16.5 million variants from the UK Biobank resource. Following replication and metaanalysis in up to 30,727 cases and 297,191 controls, we report 9 new osteoarthritis loci, in all of which the most likely causal variant is non-coding. For three loci, we detect association with biologically-relevant radiographic endophenotypes, and in five signals we identify genes that are differentially expressed in degraded compared to intact articular cartilage from osteoarthritis patients. We establish causal effects for higher body mass index, but not for triglyceride levels or type 2 diabetes liability, on osteoarthritis.Osteoarthritis (OA) is the most prevalent musculoskeletal disease and the most common form of arthritis 1 . The hallmarks of OA are degeneration of articular cartilage, remodelling of the underlying bone and synovitis 2 . A leading cause of disability worldwide, it affects 40% of individuals over the age of 70 and is associated with an increased risk of comorbidity and

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“…Protein phosphatases are pivotal enzymes in diverse eukaryotic physiological processes including cell differentiation and proliferation, cell-cell communication, and regulation of transmembrane and intracellular signaling pathways. Dysregulation of these proteins expression or activity has been documented to be linked with numerous human diseases [45,50,51], including cancer, obesity, and osteoporosis.…”

Section: Discussionmentioning

confidence: 99%

Integrative genomics analysis of eQTL and GWAS summary data identifies PPP1CB as a novel bone mineral density risk genes

Zhai

Shao

et al. 2020

Bioscience Reports

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In recent years, multiple genome-wide association studies (GWAS) have identified numerous susceptibility variants and risk genes that demonstrate significant associations with bone mineral density (BMD). However, exploring how these genetic variants contribute risk to BMD remains a major challenge. We systematically integrated two independent expression quantitative trait loci (eQTL) data (N = 1890) and GWAS summary statistical data of BMD (N = 142,487) using Sherlock integrative analysis to reveal whether expression-associated variants confer risk to BMD. By using Sherlock integrative analysis and MAGMA gene-based analysis, we found there existed 36 promising genes, for example, PPP1CB, XBP1, and FDFT1, whose expression alterations may contribute susceptibility to BMD. Through a protein–protein interaction (PPI) network analysis, we further prioritized the PPP1CB as a hub gene that has interactions with predicted genes and BMD-associated genes. Two eSNPs of rs9309664 (PeQTL = 1.42 × 10−17 and PGWAS = 1.40 × 10−11) and rs7475 (PeQTL = 2.10 × 10−6 and PGWAS = 1.70 × 10−7) in PPP1CB were identified to be significantly associated with BMD risk. Consistently, differential gene expression analysis found that the PPP1CB gene showed significantly higher expression in low BMD samples than that in high BMD samples based on two independent expression datasets (P = 0.0026 and P = 0.043, respectively). Together, we provide a convergent line of evidence to support that the PPP1CB gene involves in the etiology of osteoporosis.

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Mitogen-activated protein kinase phosphatase-1: function and regulation in bone and related tissues

Cited by 12 publications

References 141 publications

Genome-wide analyses using UK Biobank data provide insights into the genetic architecture of osteoarthritis

Genome-wide analyses using UK Biobank data provide insights into the genetic architecture of osteoarthritis

The genetic architecture of osteoarthritis: insights from UK Biobank

Integrative genomics analysis of eQTL and GWAS summary data identifies PPP1CB as a novel bone mineral density risk genes

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