Results 81 to 90 of about 19,123,678 (263)

Phase Separation of TRIM21 Modulates PTPN14 Stability to Drive Flow‐Dependent Endothelial Activation and Atherogenesis

open access: yesAdvanced Science, EarlyView.
Disturbed flow promotes the formation of TRIM21‐rich biomolecular droplets, which concentrate TRIM21 and PTPN14 and facilitate their SPRY‐FERM interaction (illustrated by the TRIM21 D355‐PTPN14 R132 salt bridge). This condensate‐driven proximity enables TRIM21 to catalyze K48‐linked polyubiquitination of PTPN14 at lysine 956, leading to proteasome ...
Xue He   +10 more
wiley   +1 more source

A retrospective nationwide analysis of evolocumab use in Sweden and its effect on low-density lipoprotein cholesterol levels

open access: yesUpsala Journal of Medical Sciences
Background: Treatment with proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors reduces low-density lipoprotein cholesterol (LDL-C) levels and decreases the incidence of major ischaemic events in clinical trials.
Maria K. Svensson   +7 more
doaj   +1 more source

Compact 9dBEs Enable Efficient and Precise Genome Editing in Mammalian Cells and In Vivo

open access: yesAdvanced Science, EarlyView.
As a compact type II‐D system, the Cas9d‐based platform holds great potential for in vivo applications. Through rational engineering, its derived base editors (9dBEs) enable efficient disease modeling while facilitating single‐vector AAV delivery for in vivo genome editing. These miniature tools offer a robust strategy for basic research and biomedical
Qingquan Xiao   +12 more
wiley   +1 more source

The E3 ubiquitin ligase c-IAP1 regulates PCSK9-mediated LDLR degradation: Linking the TNF-α pathway to cholesterol uptake [PDF]

open access: yes, 2010
Proprotein convertase subtilisin/kexin type 9 (PCSK9), in addition to LDLR (low-density lipoprotein receptor) and APOB (apolipoprotein B), is one of three loci implicated in autosomal dominant hypercholesterolaemia (ADH)^1^.
Lizhi Liu, Weiming Xu
core  

LDL-C levels.

open access: yes, 2012
LDL-C levels at baseline and 1 year (A) and small LDL particle levels at baseline and 1 year (B) stratified by treatment group and lipid GRS. Each column shows ethnicity-adjusted arithmetic (for LDL-C) or geometric (for small LDL particles) means (with ...
Alan R. Shuldiner (110828)   +13 more
core   +1 more source

Regression analysis between LDL-C levels estimated by formulas and directly measured LDL-C levels.

open access: yes, 2022
Correlations of estimated LDL-C levels by Friedewald, Sampson, Martin-Hopkins and extended Martin-Hopkins formulas with LDL-C levels directly measured by Roche, Beckman and Siemens.
Gökmen Zararsız (4385767)   +6 more
core   +1 more source

Potential of Nanoparticle‐Based Phototherapies for Future Treatment of Uveal Melanoma

open access: yesAdvanced Science, EarlyView.
This review evaluates nanoparticle‐based phototherapies for uveal melanoma, highlighting emerging strategies to enhance tumor targeting, light delivery, and treatment precision. Preclinical data indicate improved efficacy and reduced toxicity, supporting their potential to enhance localized treatment and future translational advances. (Generated by the
Emilie Lambert   +8 more
wiley   +1 more source

Irisin inhibited EC apoptosis in partial ligated carotid arteries and ox-LDL-induced HUVECs.

open access: yes, 2016
(A) Sections from the mice carotid arteries were labeled by TUNEL to detect apoptotic cells and counterstained with DAPI to detect nuclei. The yellow dotted lines indicated the lumen perimeter of the vessel.
Zheng Zhou (152309)   +16 more
core   +1 more source

THSD7A Exacerbates Atherosclerosis via Activation of Signaling Axis αvβ3/CEBPD/IL1A

open access: yesAdvanced Science, EarlyView.
THSD7A exerts pro‐inflammatory effects and exacerbates atherosclerosis. Mechanistically, THSD7A regulates endothelial cell inflammation and atherosclerosis by activating the αvβ3/CEBPD/IL1A signaling axis. THSD7A is not only a genetic marker but also a potential therapeutic target for coronary artery disease (CAD).
Jiankun Liu   +15 more
wiley   +1 more source

OAF Blocks SIAH1‐Mediated Degradation of SCPX, a Therapeutic Strategy for MASLD

open access: yesAdvanced Science, EarlyView.
This study shows OAF directly binds to SCPX and inhibits its interaction with the E3 ligase SIAH1, thereby protecting SCPX from ubiquitin‐dependent degradation and stabilizing its levels. This OAF‐SCPX axis represents a novel pathway in lipid homeostasis, highlighting OAF as a promising therapeutic candidate for MASLD.
Zongxi Li   +11 more
wiley   +1 more source

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