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Items: 1 to 20 of 187

1.

Dimerization of the transmembrane domain of amyloid precursor proteins and familial Alzheimer's disease mutants.

Gorman PM, Kim S, Guo M, Melnyk RA, McLaurin J, Fraser PE, Bowie JU, Chakrabartty A.

BMC Neurosci. 2008 Jan 30;9:17. doi: 10.1186/1471-2202-9-17.

2.

GxxxG motifs within the amyloid precursor protein transmembrane sequence are critical for the etiology of Abeta42.

Munter LM, Voigt P, Harmeier A, Kaden D, Gottschalk KE, Weise C, Pipkorn R, Schaefer M, Langosch D, Multhaup G.

EMBO J. 2007 Mar 21;26(6):1702-12. Epub 2007 Mar 1.

3.

Amyloid beta 42 peptide (Abeta42)-lowering compounds directly bind to Abeta and interfere with amyloid precursor protein (APP) transmembrane dimerization.

Richter L, Munter LM, Ness J, Hildebrand PW, Dasari M, Unterreitmeier S, Bulic B, Beyermann M, Gust R, Reif B, Weggen S, Langosch D, Multhaup G.

Proc Natl Acad Sci U S A. 2010 Aug 17;107(33):14597-602. doi: 10.1073/pnas.1003026107. Epub 2010 Aug 2.

4.

Dissociation between the processivity and total activity of γ-secretase: implications for the mechanism of Alzheimer's disease-causing presenilin mutations.

Quintero-Monzon O, Martin MM, Fernandez MA, Cappello CA, Krzysiak AJ, Osenkowski P, Wolfe MS.

Biochemistry. 2011 Oct 25;50(42):9023-35. doi: 10.1021/bi2007146. Epub 2011 Sep 30.

5.

Dimerization of the transmembrane domain of amyloid precursor protein is determined by residues around the γ-secretase cleavage sites.

Yan Y, Xu TH, Harikumar KG, Miller LJ, Melcher K, Xu HE.

J Biol Chem. 2017 Sep 22;292(38):15826-15837. doi: 10.1074/jbc.M117.789669. Epub 2017 Aug 8.

6.

Autosomal-dominant Alzheimer's disease mutations at the same codon of amyloid precursor protein differentially alter Aβ production.

Suárez-Calvet M, Belbin O, Pera M, Badiola N, Magrané J, Guardia-Laguarta C, Muñoz L, Colom-Cadena M, Clarimón J, Lleó A.

J Neurochem. 2014 Jan;128(2):330-9. doi: 10.1111/jnc.12466. Epub 2013 Oct 24.

7.

Aberrant amyloid precursor protein (APP) processing in hereditary forms of Alzheimer disease caused by APP familial Alzheimer disease mutations can be rescued by mutations in the APP GxxxG motif.

Munter LM, Botev A, Richter L, Hildebrand PW, Althoff V, Weise C, Kaden D, Multhaup G.

J Biol Chem. 2010 Jul 9;285(28):21636-43. doi: 10.1074/jbc.M109.088005. Epub 2010 May 7.

8.

beta-Secretase cleavage of the amyloid precursor protein mediates neuronal apoptosis caused by familial Alzheimer's disease mutations.

McPhie DL, Golde T, Eckman CB, Yager D, Brant JB, Neve RL.

Brain Res Mol Brain Res. 2001 Dec 16;97(1):103-13.

PMID:
11744168
9.

Familial Alzheimer's mutations within APPTM increase Aβ42 production by enhancing accessibility of ε-cleavage site.

Chen W, Gamache E, Rosenman DJ, Xie J, Lopez MM, Li YM, Wang C.

Nat Commun. 2014;5:3037. doi: 10.1038/ncomms4037.

10.

Familial Alzheimer's disease mutations inhibit gamma-secretase-mediated liberation of beta-amyloid precursor protein carboxy-terminal fragment.

Wiley JC, Hudson M, Kanning KC, Schecterson LC, Bothwell M.

J Neurochem. 2005 Sep;94(5):1189-201. Epub 2005 Jun 30.

11.

Molecular determinants and thermodynamics of the amyloid precursor protein transmembrane domain implicated in Alzheimer's disease.

Wang H, Barreyro L, Provasi D, Djemil I, Torres-Arancivia C, Filizola M, Ubarretxena-Belandia I.

J Mol Biol. 2011 May 20;408(5):879-95. doi: 10.1016/j.jmb.2011.03.028. Epub 2011 Mar 31.

12.

Amyloidogenic processing but not amyloid precursor protein (APP) intracellular C-terminal domain production requires a precisely oriented APP dimer assembled by transmembrane GXXXG motifs.

Kienlen-Campard P, Tasiaux B, Van Hees J, Li M, Huysseune S, Sato T, Fei JZ, Aimoto S, Courtoy PJ, Smith SO, Constantinescu SN, Octave JN.

J Biol Chem. 2008 Mar 21;283(12):7733-44. doi: 10.1074/jbc.M707142200. Epub 2008 Jan 16. Erratum in: J Biol Chem. 2008 May 2;283(18):12680.

13.

Evaluation of the Expression of Amyloid Precursor Protein and the Ratio of Secreted Amyloid Beta 42 to Amyloid Beta 40 in SH-SY5Y Cells Stably Transfected with Wild-Type, Single-Mutant and Double-Mutant Forms of the APP Gene for the Study of Alzheimer's Disease Pathology.

Pahrudin Arrozi A, Shukri SNS, Wan Ngah WZ, Mohd Yusof YA, Ahmad Damanhuri MH, Makpol S.

Appl Biochem Biotechnol. 2017 Nov;183(3):853-866. doi: 10.1007/s12010-017-2468-6. Epub 2017 Apr 17.

PMID:
28417423
14.

Enzymatic characteristics of I213T mutant presenilin-1/gamma-secretase in cell models and knock-in mouse brains: familial Alzheimer disease-linked mutation impairs gamma-site cleavage of amyloid precursor protein C-terminal fragment beta.

Shimojo M, Sahara N, Mizoroki T, Funamoto S, Morishima-Kawashima M, Kudo T, Takeda M, Ihara Y, Ichinose H, Takashima A.

J Biol Chem. 2008 Jun 13;283(24):16488-96. doi: 10.1074/jbc.M801279200. Epub 2008 Apr 21.

15.

Presenilin-1 mutations of leucine 166 equally affect the generation of the Notch and APP intracellular domains independent of their effect on Abeta 42 production.

Moehlmann T, Winkler E, Xia X, Edbauer D, Murrell J, Capell A, Kaether C, Zheng H, Ghetti B, Haass C, Steiner H.

Proc Natl Acad Sci U S A. 2002 Jun 11;99(12):8025-30. Epub 2002 Jun 4.

16.

Mutations in APP have independent effects on Abeta and CTFgamma generation.

Hecimovic S, Wang J, Dolios G, Martinez M, Wang R, Goate AM.

Neurobiol Dis. 2004 Nov;17(2):205-18.

PMID:
15474359
17.

Changed membrane integration and catalytic site conformation are two mechanisms behind the increased Aβ42/Aβ40 ratio by presenilin 1 familial Alzheimer-linked mutations.

Wanngren J, Lara P, Ojemalm K, Maioli S, Moradi N, Chen L, Tjernberg LO, Lundkvist J, Nilsson I, Karlström H.

FEBS Open Bio. 2014 Apr 24;4:393-406. doi: 10.1016/j.fob.2014.04.006. eCollection 2014.

18.

APP intracellular domain formation and unaltered signaling in the presence of familial Alzheimer's disease mutations.

Bergman A, Religa D, Karlström H, Laudon H, Winblad B, Lannfelt L, Lundkvist J, Näslund J.

Exp Cell Res. 2003 Jul 1;287(1):1-9.

PMID:
12799176
20.

Alzheimer's disease mutations in APP but not γ-secretase modulators affect epsilon-cleavage-dependent AICD production.

Dimitrov M, Alattia JR, Lemmin T, Lehal R, Fligier A, Houacine J, Hussain I, Radtke F, Dal Peraro M, Beher D, Fraering PC.

Nat Commun. 2013;4:2246. doi: 10.1038/ncomms3246.

PMID:
23907250

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