Cited by 146

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Sterol regulatory element binding proteins (SREBP)-1a and SREBP-2 are linked to the MAP-kinase cascade

Kotzka, Jörg, Müller-Wieland, Dirk, Roth, Gunther, Kremer, Lorena, Munck, Martina, Schürmann, Sandra, Knebel, Birgit, Krone, Wilhelm·2000·Journal of Lipid Research

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Crossref · 10.1016/s0022-2275(20)32079-4

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  • ERK1/2 signaling has been previously shown to regulate SREBP2 activity in HepG2 cells via direct phosphorylation.

    “ERK1/2 signaling has been previously shown to regulate SREBP2 activity in HepG2 cells via direct phosphorylation (Arito et al., 2008; Kotzka et al., 2004; Kotzka et al., 2000)”

    From GPR146 Deficiency Protects against Hypercholesterolemia and Atherosclerosis (2019) · cites this paper as Kotzka et al., 2000

    The Results report that MAP-kinase pathway activation increased SREBP-2 transcriptional activity in HepG2 cells, and that ERK1 or ERK2 directly phosphorylated recombinant SREBP-2 in vitro. The Abstract describes SREBP-2 as *possibly* a direct ERK1/2 substrate; it does not establish that direct phosphorylation mediates the activity change in HepG2 cells. Page numbers are not available in the supplied passages. (LLM, conf=0.88)

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  • The MEK1/ERK cascade directly phosphorylates SREBP2 at Ser-432 and Ser-455, inhibiting its sumoylation and promoting its transcription activity.

    “Previous studies in HepG2 cells showed that MEK1/ERK cascade directly phosphorylates SREBP2 at Ser-432 and Ser-455, which inhibits its sumoylation and subsequently promotes its transcription activity (Arito et al., 2008; Kotzka et al., 2004; Kotzka et al., 2000).”

    From GPR146 Deficiency Protects against Hypercholesterolemia and Atherosclerosis (2019) · cites this paper as Kotzka et al., 2000

    The Results report that ERK1 and ERK2 phosphorylated SREBP-2 on serine residues in vitro, and that activating the MAP-kinase cascade increased SREBP-2 transcriptional activity in HepG2 cells. The paper does not identify Ser-432 or Ser-455, test sumoylation, or establish that phosphorylation at those sites causes the increased activity. (LLM, conf=0.91)

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Citations

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Research works printed but not linked: 33

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Metadata

Authors
Kotzka, J., Müller-Wieland, D., Roth, G., Kremer, L., Munck, M., Schürmann, S., Knebel, B., & Krone, W.
Venue
Journal of Lipid Research
Publisher
Elsevier BV
Published
2000-01
Volume
41
Issue
1
Pages
99-108
ISSN
0022-2275
Cited by
146
References
3
Language
en

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