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Cited by 58

The DOI matches its Crossref record; 7 of the 7 references it cites were found in a registry or an index.

Neuronal human BACE1 knockin induces systemic diabetes in mice

Plucińska, Kaja, Dekeryte, Ruta, Koss, David, Shearer, Kirsty, Mody, Nimesh, Whitfield, Phillip D., Doherty, Mary K., Mingarelli, Marco, Welch, Andy, Riedel, Gernot, Delibegovic, Mirela, Platt, Bettina·2016·Diabetologia
DOI 10.1007/s00125-016-3960-1PMC PMC4901117
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Crossref · 10.1007/s00125-016-3960-1

Cites

7 of 7 references verified0 citation errors · 0 not checkable

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  • BACE1 knock-in was found to increase adipogenesis, hyperleptinemia, PTP1B, and ER stress.

    “Supporting this, BACE1 knock‐in was found to increase adipogenesis, hyperleptinemia, PTP1B, and ER stress.”

    From BACE1: More than just a β‐secretase (2022) · cites this paper as [34]

  • Through additional substrates, BACE1 has been implicated in inflammation, cardiovascular function, glucose homeostasis, and insulin signaling.

    “Through these additional substrates, BACE1 has been implicated in inflammation, cardiovascular function, glucose homeostasis, and insulin signaling”

    From BACE1: More than just a β‐secretase (2022) · cites this paper as [34]

  • In a variety of pathological conditions, including AD, cerebral amyloid angiopathy, and metabolic diseases such as type 2 diabetes and obesity, BACE1 expression and activity are increased and drive disease progression.

    “In a variety of pathological conditions, including AD, cerebral amyloid angiopathy, and metabolic diseases such as type 2 diabetes and obesity, BACE1 expression and activity are increased and drive disease progression.”

    From BACE1: More than just a β‐secretase (2022) · cites this paper as [34]

  • Pathologically elevated BACE1 expression in these cells has been implicated in the development of metabolic diseases, including type 2 diabetes, obesity, and cardiovascular disease.

    “Pathologically elevated BACE1 expression in these cells has been implicated in the development of metabolic diseases, including type 2 diabetes, obesity, and cardiovascular disease.”

    From BACE1: More than just a β‐secretase (2022) · cites this paper as [34]

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Citations

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Research works printed but not linked: 42

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  4. Mody N, Agouni A, McIlroy GD, Platt B, Delibegovic M (2011) Susceptibility to diet-induced obesity and glucose intolerance in the APP (SWE)/PSEN1 (A246E) mouse model of Alzheimer’s disease is associated with increased brain levels of protein tyrosine phosphatase 1B (PTP1B) and retinol-binding protein 4 (RBP4), and basal phosphorylation of S6 ribosomal protein. Diabetologia 54:2143–2151 · DOI
  5. Vassar R, Bennett BD, Babu-Khan S et al (1999) β-Secretase cleavage of Alzheimer’s amyloid precursor protein by the transmembrane aspartic protease BACE. Science 286:735–741 · DOI · Paper page
  6. Fukumoto H, Cheung BS, Hyman BT, Irizarry MC (2002) β-Secretase protein and activity are increased in the neocortex in Alzheimer disease. Arch Neurol 59:1381–1389 · DOI · Paper page
  7. Holsinger RMD, McLean CA, Beyreuther K, Masters CL, Evin G (2002) Increased expression of the amyloid precursor β-secretase in Alzheimer’s disease. Ann Neurol 51:783–786 · DOI · Paper page
  8. Laird FM, Cai H, Savonenko AV et al (2005) BACE1, a major determinant of selective vulnerability of the brain to amyloid-β amyloidogenesis, is essential for cognitive, emotional, and synaptic functions. J Neurosci 25:11693–11709 · DOI · Paper page
  9. Plucinska K, Crouch B, Koss D et al (2014) Knock-in of human BACE1 cleaves murine APP and reiterates Alzheimer-like phenotypes. J Neurosci 34:10710–10728 · DOI
  10. Hemming ML, Elias JE, Gygi SP, Selkoe DJ (2009) Identification of beta-secretase (BACE1) substrates using quantitative proteomics. PLoS One 4(12), E8477 · DOI
  11. Huse JT, Byant D, Yang Y et al (2003) Endoproteolysis of β-secretase (β-site amyloid precursor protein-cleaving enzyme) within its catalytic domain: a potential mechanism for regulation. J Biol Chem 278:17141–17149 · DOI
  12. Sinha S, Anderson JP, Barbour R et al (1999) Purification and cloning of amyloid precursor protein β-secretase from human brain. Nature 402:537–540 · DOI · Paper page
  13. Meakin PJ, Harper AJ, Hamilton DL et al (2012) Reduction in BACE1 decreases body weight, protects against diet-induced obesity and enhances insulin sensitivity in mice. Biochem J 441:285–295 · DOI · Paper page
  14. Guglielmotto M, Aragno M, Tamagno E et al (2012) AGEs/RAGE complex upregulates BACE1 via Nf-κB pathway activation. Neurobiol Aging 33:196.e13–196.e27 · DOI
  15. Devi L, Alldred MJ, Ginsberg SD, Ohno M (2012) Mechanisms underlying insulin deficiency-induced acceleration of β-amyloidosis in a mouse model of Alzheimer’s disease. PLoS One 7, e32792 · DOI
  16. Owen C, Lees EK, Grant L et al (2013) Inducible liver-specific knockdown of protein tyrosine phosphatase 1B improves glucose and lipid homeostasis in adult mice. Diabetologia 56:2286–2296 · DOI
  17. Platt B, Drever B, Koss D et al (2011) Abnormal cognition, sleep, EEG and brain metabolism in a novel knock-in Alzheimer mouse, PLB1. PLoS One 6, e27068 · DOI
  18. Welinder C, Ekblad L (2011) Coomassie staining as loading control in western blot analysis. J Proteome Res 10:1416–1419 · DOI · Paper page
  19. McIlroy GD, Delibegovic M, Owen C et al (2013) Fenretinide treatment prevents diet-induced obesity in association with major alterations in retinoid homeostatic gene expression in adipose, liver, and hypothalamus. Diabetes 62:825–836 · DOI
  20. Schwartz MW, Woods SC, Porte D Jr, Seeley RJ, Baskin DG (2000) Central nervous system control of food intake. Nature 404:661–671 · DOI · Paper page
  21. Mapstone M, Cheema AK, Fiandaca MS et al (2014) Plasma phospholipids identify antecedent memory impairment in older adults. Nat Med 20:415–418 · DOI
  22. Wang GX, Zhao XY, Lin JD (2015) The Brown fat secretome: metabolic functions beyond thermogenesis. Trends Endocrinol Metab 26:231–237 · DOI
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  24. Hoffmeister A, Tuennemann J, Sommerer I et al (2013) Genetic and biochemical evidence for a functional role of BACE1 in the regulation of insulin mRNA expression. Obesity 21:E626–E633 · DOI
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Metadata

Authors
Plucińska, K., Dekeryte, R., Koss, D., Shearer, K., Mody, N., Whitfield, P. D., Doherty, M. K., Mingarelli, M., Welch, A., Riedel, G., Delibegovic, M., & Platt, B.
Venue
Diabetologia
Publisher
Springer Science and Business Media LLC
Published
2016-05-02
Volume
59
Issue
7
Pages
1513-1523
ISSN
  • 0012-186X
  • 1432-0428
DOI
10.1007/s00125-016-3960-1
PMC
PMC4901117
Cited by
58
References
7
Language
en
Licence
creativecommons.org/licenses/by/4.0 (unspecified)

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