Results 251 to 260 of about 14,338,489 (301)

Radiotherapy Enhances the Oncolytic Efficacy of the Novel Oncolytic Herpesvirus VG161 and Amplifies Its Antitumor Immunity in Breast Cancer

Advanced Science, EarlyView.
RT promotes VG161 replication in BC and its immunostimulatory transgenes expression, which is mediated by the upregulation of GADD34 and HVEM caused by RT. The combination therapy with VG161 and RT increases the abundances of tumor‐infiltrating lymphocytes and elicits potent systemic antitumor immunity, thereby effectively inhibiting local tumors and ...
Lijuan Lyu, Ming Yi, Ji Chen, Zeda Zhao, Ruocen Liao, Yingnan Wang, Shengtao Hu, Jun Ding, Ronghua Zhao, William Jia, Yinan Shen, Yongchang Wei, Kongming Wu, Zhijun Dai   +13 more
wiley   +1 more source

TOLLIP Inhibits Psoriasis Progression via Suppressing PKM2‐Mediated Glycolysis in Keratinocytes

Advanced Science, EarlyView.
In this study, we identify TOLLIP as a critical regulator of psoriasis pathogenesis through its modulation of glycolytic metabolism. Our findings establish the TOLLIP‐PKM2‐glycolysis axis as a key mechanism linking metabolic reprogramming to psoriasis pathogenesis, and propose TOLLIP as a promising therapeutic target.
Xiuhuan Jiang, Guoying Miao, Na Shen, Qingxia Han, Xiaoru Han, Zichang Qiao, Kexin Feng, Zhuo Tan, Yaguang Wang, Xiuhua Liu, Chen Wu, Zhenzhen Yan   +11 more
wiley   +1 more source

Lilrb4a Suppression Reprograms Microglia to Mitigate APOE4‐Associated Amyloid Plaques and Cerebral Amyloid Angiopathy in Association With a PPAR‐Linked Pro‐Clearance State

Advanced Science, EarlyView.
Targeting Lilrb4a in Apolipoprotein E4 (APOE4)‐associated Alzheimer's disease (AD) reprograms microglia toward a beneficial, phagocytic state. Genetic deletion or antisense inhibition of Lilrb4a suppresses p‐SHP2/NF‐κB/STAT1 signaling, restores PPAR‐linked lipid and energy metabolism, and reduces amyloid plaque burden and cerebral amyloid angiopathy ...
Changxu Nie, Ruixi Yang, Xiaotong Wang, Ping Jia, Xueqi Zhang, Yaqi Dai, Xue Bai, Sijia Duan, Yufeng Li, Peng Zheng, Xin Tian, Li Jiang, Chao Wang   +12 more
wiley   +1 more source

Some of the next articles are maybe not open access.

Related searches:

Regulation of G Protein-Coupled Receptor Kinases

Trends in Cardiovascular Medicine, 2000
G protein-coupled receptor kinases (GRKs) specifically interact with the agonist-activated form of G protein-coupled receptors (GPCRs) to effect receptor phosphorylation and desensitization. Recent studies demonstrate that GRK function is a highly regulated process, and it is perhaps in this manner that a handful of GRKs (7 have been identified to date)
R B, Penn, A N, Pronin, J L, Benovic
openaire   +2 more sources

Cardiac G-Protein–Coupled Receptor Kinase 2 Ablation Induces a Novel Ca 2+ Handling Phenotype Resistant to Adverse Alterations and Remodeling After Myocardial Infarction [PDF]

Circulation, 2012
G-protein-coupled receptor kinase 2 (GRK2) is a primary regulator of β-adrenergic signaling in the heart. G-protein-coupled receptor kinase 2 ablation impedes heart failure development, but elucidation of the cellular mechanisms has not been achieved ...
Steven Houser, Philip Raake, Xiongwen Chen   +2 more
exaly   +2 more sources

G-protein-coupled receptor regulation: role of G-protein-coupled receptor kinases and arrestins

Canadian Journal of Physiology and Pharmacology, 1996
G-protein-coupled receptors (GPCRs) represent a large family of proteins that transduce extracellular signals to the interior of cells. Signalling through these receptors rapidly desensitized primarily as the consequence of receptor phosphorylation, but receptor sequestration and downregulation can also contribute to this process.
S S, Ferguson, L S, Barak, J, Zhang, M G, Caron   +3 more
openaire   +2 more sources

G protein—coupled receptor kinases

Cell, 1993
G protein‐coupled receptor kinases (GRKs) constitute a family of six mammalian serine/threonine protein kinases that phosphorylate agonist-bound, or activated, G protein‐coupled receptors (GPCRs) as their primary substrates. GRK-mediated receptor phosphorylation rapidly initiates profound impairment of receptor signaling, or desensitization.
openaire   +2 more sources

Characterization of G protein-coupled receptor kinases

2002
Publisher Summary A basic feature of most cells is the ability to dynamically regulate their responsiveness to extracellular stimuli. Numerous stimuli transmit their signals via interaction with cell surface G protein-coupled receptors (GPCRs). GPCRs are subject to three principal modes of regulation: (1) desensitization, the process by which a ...
Alexey N, Pronin, Robert P, Loudon, Jeffrey L, Benovic   +2 more
openaire   +2 more sources

Targeting G protein-coupled receptor kinases to their receptor substrates

Journal of Membrane Biology, 1997
Membrane association is essential for GRK function and because of this the GRKs have evolved complex regulatory mechanisms for associating with the membrane. Although the GRKs are highly homologous, each kinase utilizes a distinct mechanism for associating with the membrane, which makes it unique within the family.
R H, Stoffel, J A, Pitcher, R J, Lefkowitz   +2 more
openaire   +2 more sources

G-protein-coupled receptor kinases and the heart

Trends in Cardiovascular Medicine, 1995
The family of G-protein-coupled receptors includes many well-studied members, such as the adrenergic and the muscarinic acetylcholine receptors. These receptors are regulated by multiple mechanisms that serve to adapt their expression and their function to a rapidly changing environment.
openaire   +2 more sources