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Browsing publications by Professor Michael Briggs.

Newcastle AuthorsTitleYearFull text
Dan Hayman
Dr Tamara Modebadze
Sarah Charlton
Kat Cheung
Dr Jamie Soul
et al.
Increased hippocampal excitability in miR-324-null mice2021
Dr Ella Dennis
Professor Michael Briggs
Multiple epiphyseal dysplasia and related disorders: Molecular genetics, disease mechanisms, and therapeutic avenues2021
Dr Ella Dennis
Robert Jackson
Dr Dimitra Tsompani
Professor David Young
Dr Katarzyna Pirog
et al.
CRELD2 is a novel LRP1 chaperone that regulates non-canonical WNT signalling in skeletal development2020
Professor Michael Briggs
Dr Ella Dennis
Helen Dietmar
Dr Katarzyna Pirog
New developments in chondrocyte ER-stress and related diseases2020
Dr Jamie Soul
Professor Michael Briggs
Cartilage endoplasmic reticulum stress may influence the onset but not the progression of experimental osteoarthritis2019
Dr Katarzyna Pirog
Dr Ella Dennis
Robert Jackson
Dr Jamie Soul
Professor Michael Briggs
et al.
XBP1 signalling is essential for alleviating mutant protein aggregation in ER-stress related skeletal disease.2019
Dr Peter Bell
Dr Ella Dennis
Robert Jackson
Dr Anna Porter
Dr Katarzyna Pirog
et al.
Mesencephalic astrocyte-derived neurotrophic factor is an important factor in chondrocyte ER homeostasis2018
Professor Michael Briggs
Increased intracellular proteolysis reduces disease severity in an ER stress-associated dwarfism2017
Professor Michael Briggs
Dr Peter Bell
Dr Katarzyna Pirog
Pseudoachondroplasia and Multiple Epiphyseal Dysplasia: Molecular Genetics, Disease Mechanisms and Therapeutic Targets.2017
Professor Michael Briggs
ER stress: a new regulator of chondrocyte biology and cartilage health2016
Dr Beth Gibson
Professor Michael Briggs
The aggrecanopathies; an evolving phenotypic spectrum of human genetic skeletal diseases2016
Dr Ella Dennis
Dr Katarzyna Pirog
Professor Michael Briggs
The role of Creld2 in skeletal development and homeostasis2016
Dr Katarzyna Pirog
Professor Michael Briggs
Cartilage-Specific Ablation of XBP1 Signaling in Mouse Results in a Chondrodysplasia Characterized by Reduced Chondrocyte Proliferation and Delayed Cartilage Maturation and Mineralization2015
Professor Michael Briggs
Increased Classical Endoplasmic Reticulum Stress Is Sufficient to Reduce Chondrocyte Proliferation Rate in the Growth Plate and Decrease Bone Growth2015
Robert Jackson
Dr Peter Bell
Professor Michael Briggs
Molecular mechanisms provide new insight on genotype to phenotype correlations in type II collagenopathies2015
Professor Michael Briggs
Dr Peter Bell
Dr Michael Wright
Dr Katarzyna Pirog
New therapeutic targets in rare genetic skeletal diseases2015
Dr Ella Dennis
Dr Katarzyna Pirog
Professor Michael Briggs
The role of CRELD2 in skeletal development and homeostasis2015
Professor Michael Briggs
Dr Peter Bell
Dr Katarzyna Pirog
The utility of mouse models to provide information regarding the pathomolecular mechanisms in human genetic skeletal diseases: The emerging role of endoplasmic reticulum stress (Review)2015
Dr Beth Gibson
Dr Katarzyna Pirog
Professor Michael Briggs
Transgenic mice with an allelic series of aggrecan mutations model the human phenotypes2015
Dr Katarzyna Pirog
Stacy Young
Dr Peter Bell
Professor Michael Briggs
Abnormal Chondrocyte Apoptosis in the Cartilage Growth Plate is Influenced by Genetic Background and Deletion of CHOP in a Targeted Mouse Model of Pseudoachondroplasia2014
Professor Michael Briggs
Dr Peter Bell
Genotype to phenotype correlations in cartilage oligomeric matrix protein associated chondrodysplasias2014
Dr Benedetta Gualeni
Dr Peter Bell
Professor Michael Briggs
A novel transgenic mouse model of growth plate dysplasia reveals that decreased chondrocyte proliferation due to chronic ER stress is a key factor in reduced bone growth2013
Dr Peter Bell
Professor Michael Briggs
Analysis of the cartilage proteome from three different mouse models of genetic skeletal diseases reveals common and discrete disease signatures2013
Dr Peter Bell
Professor Michael Briggs
Armet/Manf and Creld2 are components of a specialized ER stress response provoked by inappropriate formation of disulphide bonds: implications for genetic skeletal diseases2013
Professor Michael Briggs
Chondrocyte ER stress as a pathogenic factor in osteoarthritis2013
Dr Katarzyna Pirog
Professor Michael Briggs
Mild myopathy is associated with COMP but not MATN3 mutations in mouse models of genetic skeletal diseases2013
Dr Katarzyna Pirog
Professor Michael Briggs
Mutant chondrocytes are characterised by altered cell shape and changes to the organisation of primary cilia in a genetic mouse model of mild pseudoachondroplasia2013
Dr Katarzyna Pirog
Professor Michael Briggs
A novel form of chondrocyte stress is triggered by a COMP mutation causing pseudoachondroplasia2012
Dr Peter Bell
Dr Katarzyna Pirog
Professor Michael Briggs
Loss of matrilin 1 does not exacerbate the skeletal phenotype in a mouse model of multiple epiphyseal dysplasia caused by a Matn3 V194D mutation2012
Professor Michael Briggs
Pseudoachondroplasia and multiple epiphyseal dysplasia: A 7-year comprehensive analysis of the known disease genes identify novel and recurrent mutations and provides an accurate assessment of their relative contribution2012
Professor Michael Briggs
Recurrent Dominant Mutations Affecting Two Adjacent Residues in the Motor Domain of the Monomeric Kinesin KIF22 Result in Skeletal Dysplasia and Joint Laxity (vol 89, pg 769, 2011)2012
Professor Michael Briggs
Recurrent Dominant Mutations Affecting Two Adjacent Residues in the Motor Domain of the Monomeric Kinesin KIF22 Result in Skeletal Dysplasia and Joint Laxity2011
Dr Katarzyna Pirog
Professor Michael Briggs
A mouse model offers novel insights into the myopathy and tendinopathy often associated with pseudoachondroplasia and multiple epiphyseal dysplasia2010
Dr Peter Bell
Professor Michael Briggs
An unfolded protein response is the initial cellular response to the expression of mutant matrilin-3 in a mouse model of multiple epiphyseal dysplasia2010
Professor Michael Briggs
Correlating endoplasmic reticulum stress with the onset of disease phenotype in chondrodysplasias2010
Professor Michael Briggs
Molecular dissection of the unfolded protein response in hypertrophic chondrocytes2010
Dr Katarzyna Pirog
Professor Michael Briggs
Skeletal Dysplasias Associated with Mild Myopathy-A Clinical and Molecular Review2010
Professor Michael Briggs
Structural ad functional investigations of Matrillin-1 a-domains reveal insights into their role in cartilage ECM assembly2010
Professor Michael Briggs
The unfolded protein response and its relevance to connective tissue diseases2010
Professor Michael Briggs
Type IX Collagen Gene Mutations can result in Multiple Epiphyseal Dysplasia that is associated with Osteochondritis Dissecans and a Mild Myopathy2010
Dr Stuart Tompson
Professor Michael Briggs
A Recessive Skeletal Dysplasia, SEMD Aggrecan Type, Results from a Missense Mutation Affecting the C-Type Lectin Domain of Aggrecan2009
Professor Michael Briggs
Collagen XXVII mutations cause a lung phenotype and plays a role in growth plate architecture2009
Professor Michael Briggs
Genetic background influences the severity of chondrodysplasia phenotype2009
Professor Michael Briggs
Targeted induction of endoplasmic reticulum stress induces cartilage pathology2009
Professor Michael Briggs
Targeted type XXVII collagen mutations cause lung and skeletal phenotypes2008
Professor Michael Briggs
Collagen XXVII is developmentally regulated and forms thin fibrillar structures distinct from those of classical vertebrate fibrillar collagens2007
Professor Michael Briggs
Decreased chondrocyte proliferation and dysregulated apoptosis in the cartilage growth plate are key features of a murine model of epiphyseal dysplasia caused by a matn3 mutation2007
Professor Michael Briggs
Gene targeting collagen XXVII2007
Professor Michael Briggs
Genetic background influences the severity of growth plate dysplasia in a mouse model of pseudoachondroplasia2007
Dr Katarzyna Pirog
Professor Michael Briggs
Reduced cell proliferation and increased apoptosis are significant pathological mechanisms in a murine model of mild pseudoachondroplasia resulting from a mutation in the C-terminal domain of COMP2007
Professor Michael Briggs
Structural and functional characterization of recombinant matrilin-3 A-domain and implications for human genetic bone diseases2007
Professor Michael Briggs
The effects of an MCDS-causing mutation on chondrocyte proliferation in mouse growth plate2007
Professor Michael Briggs
The genetics of otosclerosis: pedigree studies and linkage analysis2007
Professor Michael Briggs
A Knockin mouse model for a collagen type X NC1 domain mutation associated with metaphyseal chondrodysplasia-type Schmid2006
Professor Michael Briggs
A matrilin-3 multiple epiphyseal dysplasia knockin mouse model2006
Professor Michael Briggs
Characterization of collagen XXVII, a new collagen with a domain structure homologous to the fibrillar collagens2006
Professor Michael Briggs
T583M COMP knockin mouse - a model of mild pseudoachondroplasia resulting from C-terminal COMP mutation2006
Professor Michael Briggs
A disorder resembling pseudoachondroplasia but without COMP mutation2005
Professor Michael Briggs
A knock-in mouse model for a collagen type X NC1 domain mutation associated with metaphyseal chondrodysplasia type Schmid (MCDS)2005
Professor Michael Briggs
A knock-in mouse model for a collagen type X NC1 domain mutation associated with metaphyseal chondrodysplasia-type Schmid2005
Professor Michael Briggs
Multiple epiphyseal dysplasia mutations in MATN3 cause misfolding of the A-domain and prevent secretion of mutant matrilin-32005
Professor Michael Briggs
Mutations in the known genes are not the major cause of MED; distinctive phenotypic entities among patients with no identified mutations2005
Professor Michael Briggs
Novel and recurrent mutations in the C-terminal domain of COMP cluster in two distinct regions and result in a spectrum of phenotypes within the pseudoachondroplasia – multiple epiphyseal dysplasia disease group2005
Professor Michael Briggs
Review: Clinical variability and genetic heterogeneity in multiple epiphyseal dysplasia2003
Professor Michael Briggs
Structural and functional changes in collagen IX due to a MED mutation2003
Professor Michael Briggs
Pseudoachondroplasia and multiple epiphyseal dysplasia: Mutation review, molecular interactions, and genotype to phenotype correlations2002
Professor Michael Briggs
Cartilage oligomeric matrix protein interacts with type IX collagen, and disruptions to these interactions identify a pathogenetic mechanism in a bone dysplasia family2001
Professor Michael Briggs
Clinical and radiographic features of multiple epiphyseal dysplasia not linked to the COMP or type IX collagen genes2001
Professor Michael Briggs
Multiple epiphyseal dysplasia: radiographic abnormalities correlated with genotype2001
Professor Michael Briggs
Professor John Loughlin
Mutations in the vWFA domain of matrilin-3 cause multiple epiphyseal dysplasia2001
Professor Michael Briggs
Matthew Wright
Update from the collaborative study of genetic diagnosis for skeletal dysplasias2001
Professor Michael Briggs
Exon skipping mutation in the COL9A2 gene in a family with multiple epiphyseal dysplasia2000
Professor Michael Briggs
Identification in vitreous and molecular cloning of opticin, a novel member of the family of leucine-rich repeat proteins of the extracellular matrix2000
Professor Michael Briggs
Molecular diagnosis is important to confirm suspected pseudoachondroplasia2000
Professor Michael Briggs
Screening for mutations in cartilage ECM genes2000
Professor Michael Briggs
Clinical variability and genetic heterogeneity in multiple epiphyseal dysplasia1999
Professor Michael Briggs
COMP gene mutations result in abnormal collagen fibril morphology1999
Professor John Loughlin
Professor Michael Briggs
Identification of novel pro-alpha 2(IX) collagen gene mutations in two families with distinctive olgo-epiphyseal forms of multiple epiphyseal dysplasia1999
Professor Michael Briggs
Trinucleotide expansion mutations in the cartilage oligomeric matrix protein (COMP) gene1999