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Armet/Manf and Creld2 are components of a specialized ER stress response provoked by inappropriate formation of disulphide bonds: implications for genetic skeletal diseases.

Hartley CL, Edwards S, Mullan L, Bell PA, Fresquet M, Boot-Handford RP, Briggs MD.

Hum Mol Genet. 2013 Dec 20;22(25):5262-75. doi: 10.1093/hmg/ddt383. Epub 2013 Aug 15.


An unfolded protein response is the initial cellular response to the expression of mutant matrilin-3 in a mouse model of multiple epiphyseal dysplasia.

Nundlall S, Rajpar MH, Bell PA, Clowes C, Zeeff LA, Gardner B, Thornton DJ, Boot-Handford RP, Briggs MD.

Cell Stress Chaperones. 2010 Nov;15(6):835-49. doi: 10.1007/s12192-010-0193-y. Epub 2010 Apr 30.


Transcriptional profiling of chondrodysplasia growth plate cartilage reveals adaptive ER-stress networks that allow survival but disrupt hypertrophy.

Cameron TL, Bell KM, Tatarczuch L, Mackie EJ, Rajpar MH, McDermott BT, Boot-Handford RP, Bateman JF.

PLoS One. 2011;6(9):e24600. doi: 10.1371/journal.pone.0024600. Epub 2011 Sep 15.


Loss of matrilin 1 does not exacerbate the skeletal phenotype in a mouse model of multiple epiphyseal dysplasia caused by a Matn3 V194D mutation.

Bell PA, Piróg KA, Fresquet M, Thornton DJ, Boot-Handford RP, Briggs MD.

Arthritis Rheum. 2012 May;64(5):1529-39. doi: 10.1002/art.33486.


Multiple epiphyseal dysplasia mutations in MATN3 cause misfolding of the A-domain and prevent secretion of mutant matrilin-3.

Cotterill SL, Jackson GC, Leighton MP, Wagener R, Mäkitie O, Cole WG, Briggs MD.

Hum Mutat. 2005 Dec;26(6):557-65.


A novel form of chondrocyte stress is triggered by a COMP mutation causing pseudoachondroplasia.

Suleman F, Gualeni B, Gregson HJ, Leighton MP, Piróg KA, Edwards S, Holden P, Boot-Handford RP, Briggs MD.

Hum Mutat. 2012 Jan;33(1):218-31. doi: 10.1002/humu.21631. Epub 2011 Nov 17.


Characterization of the Role of MANF in Regulating the Secretion of CRELD2.

Oh-hashi K, Norisada J, Hirata Y, Kiuchi K.

Biol Pharm Bull. 2015;38(5):722-31. doi: 10.1248/bpb.b14-00825.


A Comparative Analysis of the Molecular Features of MANF and CDNF.

Norisada J, Hirata Y, Amaya F, Kiuchi K, Oh-hashi K.

PLoS One. 2016 Jan 28;11(1):e0146923. doi: 10.1371/journal.pone.0146923. eCollection 2016.


Characterization of V-ATPase inhibitor-induced secretion of cysteine-rich with EGF-like domains 2.

Oh-hashi K, Kanamori Y, Hirata Y, Kiuchi K.

Cell Biol Toxicol. 2014 Jun;30(3):127-36. doi: 10.1007/s10565-014-9274-5. Epub 2014 Apr 1.


Armet, a UPR-upregulated protein, inhibits cell proliferation and ER stress-induced cell death.

Apostolou A, Shen Y, Liang Y, Luo J, Fang S.

Exp Cell Res. 2008 Aug 1;314(13):2454-67. doi: 10.1016/j.yexcr.2008.05.001. Epub 2008 May 13.


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 mutation.

Leighton MP, Nundlall S, Starborg T, Meadows RS, Suleman F, Knowles L, Wagener R, Thornton DJ, Kadler KE, Boot-Handford RP, Briggs MD.

Hum Mol Genet. 2007 Jul 15;16(14):1728-41. Epub 2007 May 21.


Role of an ER stress response element in regulating the bidirectional promoter of the mouse CRELD2 - ALG12 gene pair.

Oh-Hashi K, Koga H, Ikeda S, Shimada K, Hirata Y, Kiuchi K.

BMC Genomics. 2010 Nov 25;11:664. doi: 10.1186/1471-2164-11-664.


Increased classical endoplasmic reticulum stress is sufficient to reduce chondrocyte proliferation rate in the growth plate and decrease bone growth.

Kung LH, Rajpar MH, Preziosi R, Briggs MD, Boot-Handford RP.

PLoS One. 2015 Feb 18;10(2):e0117016. doi: 10.1371/journal.pone.0117016. eCollection 2015.


Targeted induction of endoplasmic reticulum stress induces cartilage pathology.

Rajpar MH, McDermott B, Kung L, Eardley R, Knowles L, Heeran M, Thornton DJ, Wilson R, Bateman JF, Poulsom R, Arvan P, Kadler KE, Briggs MD, Boot-Handford RP.

PLoS Genet. 2009 Oct;5(10):e1000691. doi: 10.1371/journal.pgen.1000691. Epub 2009 Oct 16.


Endoplasmic reticulum (ER) stress inducible factor cysteine-rich with EGF-like domains 2 (Creld2) is an important mediator of BMP9-regulated osteogenic differentiation of mesenchymal stem cells.

Zhang J, Weng Y, Liu X, Wang J, Zhang W, Kim SH, Zhang H, Li R, Kong Y, Chen X, Shui W, Wang N, Zhao C, Wu N, He Y, Nan G, Chen X, Wen S, Zhang H, Deng F, Wan L, Luu HH, Haydon RC, Shi LL, He TC, Shi Q.

PLoS One. 2013 Sep 3;8(9):e73086. doi: 10.1371/journal.pone.0073086. eCollection 2013.


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 COMP.

Piróg-Garcia KA, Meadows RS, Knowles L, Heinegård D, Thornton DJ, Kadler KE, Boot-Handford RP, Briggs MD.

Hum Mol Genet. 2007 Sep 1;16(17):2072-88. Epub 2007 Jun 22.


Multiple functions of the first EGF domain in matrilin-3: Secretion and endoplasmic reticulum stress.

Wang YC, Liu JS, Chen JY, Wu SQ, Wang GR, Nie J, Zhang SK, Guo QL, Luo JM.

Int J Mol Med. 2015 Dec;36(6):1648-56. doi: 10.3892/ijmm.2015.2377. Epub 2015 Oct 15.


COMP mutations, chondrocyte function and cartilage matrix.

Hecht JT, Hayes E, Haynes R, Cole WG.

Matrix Biol. 2005 Jan;23(8):525-33. Epub 2004 Nov 18.


Biosynthesis and secretion of mouse cysteine-rich with EGF-like domains 2.

Oh-hashi K, Kunieda R, Hirata Y, Kiuchi K.

FEBS Lett. 2011 Aug 4;585(15):2481-7. doi: 10.1016/j.febslet.2011.06.029. Epub 2011 Jun 30.

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