Results 41 to 50 of about 24,989 (236)

The receptor kinase family: primary structure of rhodopsin kinase reveals similarities to the beta-adrenergic receptor kinase. [PDF]

Proceedings of the National Academy of Sciences, 1991
Light-dependent deactivation of rhodopsin as well as homologous desensitization of beta-adrenergic receptors involves receptor phosphorylation that is mediated by the highly specific protein kinases rhodopsin kinase (RK) and beta-adrenergic receptor kinase (beta ARK), respectively. We report here the cloning of a complementary DNA for RK.
Lorenz, W, Inglese, J, Palczewski, K, Onorato, JJ, Caron, MG, Lefkowitz, RJ   +5 more
openaire   +2 more sources

Norepinephrine Regulation of Adrenergic Receptor Expression, 5’ AMP-Activated Protein Kinase Activity, and Glycogen Metabolism and Mass in Male Versus Female Hypothalamic Primary Astrocyte Cultures

ASN Neuro, 2020
Norepinephrine (NE) control of hypothalamic gluco-regulation involves astrocyte-derived energy fuel supply. In male rats, exogenous NE regulates astrocyte glycogen metabolic enzyme expression in vivo through 5’-AMP-activated protein kinase (AMPK ...
Mostafa M. H. Ibrahim, Khaggeswar Bheemanapally, Paul W. Sylvester, Karen P. Briski   +3 more
doaj   +1 more source

Purification and characterization of the beta-adrenergic receptor kinase.

Journal of Biological Chemistry, 1987
The beta-adrenergic receptor kinase (beta-ARK) is a recently discovered enzyme which specifically phosphorylates the agonist-occupied form of the beta-adrenergic receptor (beta-AR) as well as the light-bleached form of rhodopsin. beta-ARK is present in a wide variety of mammalian tissues.
J L, Benovic, F, Mayor, C, Staniszewski, R J, Lefkowitz, M G, Caron   +4 more
openaire   +2 more sources

Targeting the ARRDC3–DRP1 Axis via hUMSC‐Derived Exosomal CRYAB for Neuroprotection in Cerebral Ischemia/Reperfusion Injury

Advanced Healthcare Materials, EarlyView.
Intranasally administered hUMSC‐derived exosomes modulate the CRYAB–ARRDC3–Drp1 axis, alleviating mitochondrial dysfunction and ferroptosis, enhancing neuronal survival, reducing oxidative stress, and promoting functional recovery in ischemia‐reperfusion injury, offering a promising therapeutic strategy for ischemic stroke.
Rong ji, Zengyu Zhang, Zhuohang Liu, Kaicheng Yang, Xueyu Mao, Min Chu, Yong Wang, Jing Zhao   +7 more
wiley   +1 more source

Amyloid β Instigates Cardiac Neurotrophic Signaling Impairment, Driving Alzheimer's Associated Heart Disease

Advanced Science, EarlyView.
This research identified cardiac amyloid pathology, neurotrophic factor depletion, and reduced myocardial nerve function in a transgenic model of cerebral amyloidosis (Tg2576), Aβ‐challenged cardiomyocytes, and in human AD heart tissue. These findings carry significant diagnostic and therapeutic implications, emphasizing the role of neuro‐signaling ...
Andrea Elia, Rebecca Parodi‐Rullan, Rafael Vazquez‐Torres, Ashley Carey, Huaqing Zhao, Sabzali Javadov, Silvia Fossati   +6 more
wiley   +1 more source

Agonist-dependent phosphorylation of the alpha 2-adrenergic receptor by the beta-adrenergic receptor kinase.

Journal of Biological Chemistry, 1987
Desensitization of the beta-adrenergic receptor, a receptor which is coupled to the stimulation of adenylate cyclase, may be regulated via phosphorylation by a unique protein kinase. This recently discovered enzyme, known as the beta-adrenergic receptor kinase, only phosphorylates the agonist-occupied form of the beta-adrenergic receptor.
BENOVIC J. L, REGAN J. W, MATSUI H, MAYOR F. JR, LEEB LUNDBERG F. L. M, CARON M. G, LEFKOWITZ R. J., COTECCHIA, Susanna   +7 more
openaire   +2 more sources

β-Adrenergic Receptor Kinase-1 Levels in Catecholamine-Induced Myocardial Hypertrophy [PDF]

Hypertension, 1999
Abstract —Pressure overload ventricular hypertrophy is accompanied by dysfunctional β-adrenergic receptor signaling due to increased levels of the β-adrenergic receptor kinase-1, which phosphorylates and desensitizes β-adrenergic receptors.
G. Iaccarino, P. C. Dolber, R. J. Lefkowitz, W. J. Koch   +3 more
openaire   +4 more sources

OTUD6A in Airway Epithelial Cells Exacerbates Allergic Asthma by Promoting Airway Inflammation and Airway Remodeling Through Deubiquitination of hResistin/mRELMα

Advanced Science, EarlyView.
This study elucidates a novel mechanistic role of the deubiquitinase OTUD6A in asthma pathogenesis, uncovering its regulatory function in airway inflammation and airway remodeling through the stabilization of hResistin/mRELMα. This study offers a novel regulatory axis (OTUD6A‐hResistin/mRELMα) in asthma pathogenesis and OTUD6A inhibition as a potential
Weiting Pan, Xinru Xi, Wei Dai, Tingfang Xiao, Yeqing Chen, Xuanyu Chen, Xiangting Ge, Chengguang Zhao, Hui Zhang, Yali Zhang, Weixi Zhang   +10 more
wiley   +1 more source

β‐Adrenergic Signaling Promotes Anti‐Tumor Immunity in TP53‐mutant Oral Squamous Cell Carcinoma

Advanced Science, EarlyView.
β‐adrenergic stimulation enhances anti‐tumor immunity in TP53‐deficient oral squamous cell carcinoma by inducing tumor‐derived secretion of CXCL10, which attracts and activates cytotoxic CD8+ T cells. The findings demonstrate that β‐adrenergic signaling alters tumor–immune interactions via CXCL10‐mediated paracrine activation, revealing a neuro‐immune ...
Frederico O. Gleber‐Netto, Deborah Silverman, Tongxin Xie, Shamima Akhter, Nicole R. Vaughn, Adewale Adebayo, Kala Chand Debnath, Shorook Naara, Shajedul Islam, Erik Knutsen, Emily Lorin Ashkin, Simone Anfossi, Sara Leahey, Patrick Hwu, Sebastien Talbot, Erica K Sloan, Robert Saddawi‐Konefka, Roberto Rangel, Jeffrey N. Myers, George A. Calin, Moran Amit   +20 more
wiley   +1 more source

Therapeutic Gases in Biomedicine: Updates on Nitric Oxide and Beyond

Advanced Science, EarlyView.
Therapeutic gases, including NO, CO, H2S, H2, CO2, O2, and Xe, play vital roles in cellular signaling and repair. This review highlights the emerging carriers and delivery systems that enable controlled, localized gas release for diagnostic and therapeutic applications.
Syed Muntazir Andrabi, Navatha Shree Sharma, Imran Ibn Gani Rather, S. M. Shatil Shahriar, Jingwei Xie   +4 more
wiley   +1 more source