anti-Myosin Regulatory Light Chain Interacting Protein (MYLIP) Antikörper

Zebrafish Myosin Regulatory Light Chain Interacting Protein (MYLIP) Interaktionspartner

Human Myosin Regulatory Light Chain Interacting Protein (MYLIP) Interaktionspartner

1. the effects caused by human inducible degrader of the low-density lipoprotein expression are LDLR (zeige LDLR Antikörper)- dependent given the unchanged plasma lipids in LAhB mice lacking low-density lipoprotein receptor (zeige LDLR Antikörper)

2. The long noncoding RNA RP1 (zeige STK19 Antikörper)-13D10.2 may contribute to LDL cholesterol levels in response to statins.

3. Specifically, loss of IDOL increases LDLR (zeige LDLR Antikörper) distribution in the hepatic cell, and subsequently reduces serum LDL-C levels in dyslipidemic patients

4. Data suggest inducible expression of IDOL is subject to robust, rapid regulation by process that is sensitive to deubiquitinase inhibition in human/mouse cell lines and primary human cells; transcriptional induction of IDOL leads to degradation of LDLR (zeige LDLR Antikörper).

5. Identify USP2 (zeige USP2 Antikörper) as a novel regulator of lipoprotein clearance owing to its ability to control ubiquitylation-dependent degradation of the LDLR (zeige LDLR Antikörper) by IDOL.

6. The study identified MARCH6 (zeige MARCH6 Antikörper) as a negative regulator of SREBP2 (zeige SREBF2 Antikörper)-mediated transcription and described an unexpected E3 circuit functionally linking MARCH6 (zeige MARCH6 Antikörper) and IDOL to limit uptake of low-density lipoprotein via the LDLR (zeige LDLR Antikörper) pathway.

7. IDOL N342S Variant, Atherosclerosis Progression and Cardiovascular Disorders in the Italian General Population.

8. study indicates that MYLIP p.N342S might be a pharmacogenetic marker for lipid-lowering therapy in patients with FH.

9. Liver-specific expression of dominant-active IDOL is associated with hypercholesterolemia and a marked elevation in atherosclerotic lesions in transgenic mice.

10. evidence for the existence of an LXR (zeige NR1H3 Antikörper)-IDOL-mediated internalization pathway for the LDLR (zeige LDLR Antikörper) that is distinct from that used for lipoprotein uptake

Mouse (Murine) Myosin Regulatory Light Chain Interacting Protein (MYLIP) Interaktionspartner

1. describe the recently generated mouse model, L-sIDOL Tg mice, which express a dominant active form of Inducible Degrader Of the Low-density lipoprotein receptor (zeige LDLR Antikörper) (IDOL) in a liver-specific manner. This murine model offers significant advantages over previously established models for the study of hypercholesterolemia and atherosclerosis.

2. the effects caused by human inducible degrader of the low-density lipoprotein expression are LDLR (zeige LDLR Antikörper)- dependent given the unchanged plasma lipids in LAhB mice lacking low-density lipoprotein receptor (zeige LDLR Antikörper)

3. Suggest Idol as a gatekeeper of LDLR (zeige LDLR Antikörper)-dependent ApoE (zeige APOE Antikörper) and Abeta (zeige APP Antikörper) clearance in the brain and a potential enzyme target for therapeutic intervention in Alzheimer disease.

4. Estradiol-treatment led to impaired contractile function in male cardiomyocytes only, which was characterized by increased Mylip mRNA and protein levels, and decreased myosin regulatory light chain protein.

5. These data identify the IDOL-LDLR (zeige LDLR Antikörper) interaction as an evolutionarily conserved mechanism for the regulation of lipid uptake and suggest that this interaction could potentially be exploited for the pharmacologic modulation of lipid metabolism.

6. Data show that NPC1 (zeige NPC1 Antikörper) deficiency has a major impact on VLDL metabolism in Apoe (zeige APOE Antikörper)(-/-) mice through modulation of hepatic LDL-R protein levels, and a modest one on Pcsk9 (zeige PCSK9 Antikörper) and Idol induction.

7. Data show that the identification of VLDLR (zeige VLDLR Antikörper) and ApoER2 (zeige LRP8 Antikörper) as Idol(Mylip) targets suggests potential roles for this LXR (zeige NR1H3 Antikörper)-inducible E3 ligase in the central nervous system in addition to lipid metabolism.

8. study shows the LXR (zeige NR1H3 Antikörper)-Idol(Mylip)-LDLR (zeige LDLR Antikörper) axis defines a complementary pathway to sterol response element-binding proteins for sterol regulation of cholesterol uptake