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Browsing publications by Dr Peter Bell.

Newcastle AuthorsTitleYearFull text
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
Dr Peter Bell
Dr Katarzyna Pirog
Pseudoachondroplasia and Multiple Epiphyseal Dysplasia: Molecular Genetics, Disease Mechanisms and Therapeutic Targets.2017
Dr Peter Bell
Robert Jackson
Dr Katarzyna Pirog
Importance of glycosylation state and aggregation in ER-associated degradation of mutant matrilin proteins and induction of UPR2015
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 Peter Bell
Dr Benedetta Gualeni
Dr Katarzyna Pirog
Reverse genetics approach in search for the novel MED locus2015
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 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
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
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