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

Zebrafish Myosin Regulatory Light Chain Interacting Protein (MYLIP) interaction partners

1. essential for embryonic development, with a role in the extensive cell movements associated with gastrulation

Human Myosin Regulatory Light Chain Interacting Protein (MYLIP) interaction partners

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

2. The long noncoding RNA RP1-13D10.2 may contribute to LDL cholesterol levels in response to statins.

3. Specifically, loss of IDOL increases LDLR 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.

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

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

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

8. Several lipid-related gene polymorphisms interact with overweight/obesity to modulate blood pressure levels.

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

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

11. evidence for the existence of an LXR-IDOL-mediated internalization pathway for the LDLR that is distinct from that used for lipoprotein uptake

12. Results show that IDOL contributes to variation in circulating levels of LDL-C.

13. IDOL is recruited to plasma membrane by low-density lipoprotein receptor (LDLR), promotes LDLR internalization in the absence of clathrin or caveolae, and facilitates LDLR degradation by shuttling it into the multivesicular body protein-sorting pathway

14. MYLIP rs3757354 SNP is associated with serum TC, HDL-C and ApoAI levels in the Bai Ku Yao and Han populations. But the association is different between the two ethnic groups.

15. No association of the MYLIP rs9370867 genotypes with lipid profile, hemodynamic data, and coronary angiographic data was in a Brazilian population.

16. FGF21 also enhanced expression of Canopy2 (Cnpy2)/MIR-interacting Saposin-like protein (Msap) that is known to interact with Mylip/Idol.

17. expression levels rise with increasing age in hearts of men

18. both the FERM and RING domains are required for promoting lysosomal degradation of the LDLR by IDOL.

19. N342S MYLIP polymorphism is associated with high total cholesterol and increased LDL receptor degradation in humans

20. identify the IDOL-UBE2D complex as an important determinant of LDLR activity, and provide insight into molecular mechanisms underlying the regulation of cholesterol uptake

Mouse (Murine) Myosin Regulatory Light Chain Interacting Protein (MYLIP) interaction partners

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 (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- dependent given the unchanged plasma lipids in LAhB mice lacking low-density lipoprotein receptor

3. Suggest Idol as a gatekeeper of LDLR-dependent ApoE and Abeta 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 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 deficiency has a major impact on VLDL metabolism in Apoe(-/-) mice through modulation of hepatic LDL-R protein levels, and a modest one on Pcsk9 and Idol induction.

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

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