scholarly journals Cyclic Adenosine Monophosphate-dependent Phosphorylation of Specific Fat Cell Membrane Proteins by an Endogenous Membrane-bound Protein Kinase

1974 ◽  
Vol 249 (21) ◽  
pp. 6854-6865 ◽  
Author(s):  
Kwen-Jen Chang ◽  
Norman A. Marcus ◽  
Pedro Cuatrecasas
Keyword(s):  
Protein Kinase ◽  
Membrane Proteins ◽  
Cell Membrane ◽  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate ◽  
Fat Cell ◽  
Cell Membrane Proteins ◽  
Membrane Bound

scholarly journals LEVEL OF MEMBRANE-BOUND HEMOGLOBIN AND RED-CELL MEMBRANE PROTEINS IN PATIENTS WITH ESSENTIAL HYPERTENSION COMPLICATED AND NOT COMPLICATED WITH METABOLIC SYNDROME

2016 ◽  
Vol 1 (4) ◽  
pp. 61-67
Author(s):  
Горохова ◽  
Viktoriya Gorokhova ◽  
Корякина ◽  
Larisa Koryakina ◽  
Бабушкина ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Essential Hypertension ◽  
Membrane Proteins ◽  
Cell Membrane ◽  
Functional Organization ◽  
High Density Lipoproteins ◽  
Red Cell ◽  
Red Cell Membrane ◽  
Cell Membrane Proteins ◽  
Membrane Bound

We studied the effect of different levels of membrane-bound hemoglobin on the level of red-cell membrane proteins and also their interrelation in patients with essential hypertension with and without metabolic syndrome. It was found that high membrane-bound hemoglobin is closely related to the low level of high-density lipoproteins and high level of low-density lipoproteins in patients with essential hypertension complicated with metabolic syndrome. In patients with essential hypertension not complicated with metabolic syndrome high membrane-bound hemoglobin is related to the increased prothrombin time and decreased blood urea nitrogen. In patients with essential hypertension com-plicated with metabolic syndrome high membrane-bound hemoglobin significantly influences the level of membrane contractile proteins (actin, tropomiosine). In patients with essential hypertension without metabolic syndrome high membrane-bound hemoglobin is accompanied by the decrease of structural and integral membrane proteins levels (anion-transport protein and protein 4.1). As the result of quantitative changes in these proteins and change in their interrelations in patients with ssential hypertension complicated with metabolic syndrome more intensive disorders of structural and functional organization of red-cell membrane can appear.

Polydatin Attenuates Carbachol-induced Contraction of Guinea Pig Gallbladder

2019 ◽  
Vol 18 (1) ◽  
pp. 34-38
Author(s):  
Chen Lei ◽  
Pan Xiang ◽  
Shen Yonggang ◽  
Song Kai ◽  
Zhong Xingguo ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Guinea Pig ◽  
Smooth Muscles ◽  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate ◽  
Cyclic Guanosine Monophosphate ◽  
Guanosine Monophosphate ◽  
Dependent Manner ◽  
Underlying Mechanisms ◽  
Dose Dependent

The aim of this study was to determine whether polydatin, a glucoside of resveratrol isolated from the root of Polygonum cuspidatum, warranted development as a potential therapeutic for ameliorating the pain originating from gallbladder spasm disorders and the underlying mechanisms. Guinea pig gallbladder smooth muscles were treated with polydatin and specific inhibitors to explore the mechanisms underpinning polydatin-induced relaxation of carbachol-precontracted guinea pig gallbladder. Our results shown that polydatin relaxed carbachol-induced contraction in a dose-dependent manner through the nitric oxide/cyclic guanosine monophosphate/protein kinase G and the cyclic adenosine monophosphate/protein kinase A signaling pathways as well as the myosin light chain kinase and potassium channels. Our findings suggested that there was value in further exploring the potential therapeutic use of polydatin in gallbladder spasm disorders.

scholarly journals Role of Long Non-Coding RNAs and the Molecular Mechanisms Involved in Insulin Resistance

2021 ◽  
Vol 22 (14) ◽  
pp. 7256
Author(s):  
Vianet Argelia Tello-Flores ◽  
Fredy Omar Beltrán-Anaya ◽  
Marco Antonio Ramírez-Vargas ◽  
Brenda Ely Esteban-Casales ◽  
Napoleón Navarro-Tito ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Protein Kinase ◽  
Molecular Mechanisms ◽  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate ◽  
Biological Species ◽  
Necrosis Factor Alpha ◽  
Polypyrimidine Tract Binding Protein ◽  
Non Coding Rnas

Long non-coding RNAs (lncRNAs) are single-stranded RNA biomolecules with a length of >200 nt, and they are currently considered to be master regulators of many pathological processes. Recent publications have shown that lncRNAs play important roles in the pathogenesis and progression of insulin resistance (IR) and glucose homeostasis by regulating inflammatory and lipogenic processes. lncRNAs regulate gene expression by binding to other non-coding RNAs, mRNAs, proteins, and DNA. In recent years, several mechanisms have been reported to explain the key roles of lncRNAs in the development of IR, including metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), imprinted maternal-ly expressed transcript (H19), maternally expressed gene 3 (MEG3), myocardial infarction-associated transcript (MIAT), and steroid receptor RNA activator (SRA), HOX transcript antisense RNA (HOTAIR), and downregulated Expression-Related Hexose/Glucose Transport Enhancer (DREH). LncRNAs participate in the regulation of lipid and carbohydrate metabolism, the inflammatory process, and oxidative stress through different pathways, such as cyclic adenosine monophosphate/protein kinase A (cAMP/PKA), phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT), polypyrimidine tract-binding protein 1/element-binding transcription factor 1c (PTBP1/SREBP-1c), AKT/nitric oxide synthase (eNOS), AKT/forkhead box O1 (FoxO1), and tumor necrosis factor-alpha (TNF-α)/c-Jun-N-terminal kinases (JNK). On the other hand, the mechanisms linked to the molecular, cellular, and biochemical actions of lncRNAs vary according to the tissue, biological species, and the severity of IR. Therefore, it is essential to elucidate the role of lncRNAs in the insulin signaling pathway and glucose and lipid metabolism. This review analyzes the function and molecular mechanisms of lncRNAs involved in the development of IR.

scholarly journals Novel autoantibodies against muscle-cell membrane proteins in patients with myositis

1996 ◽  
Vol 39 (11) ◽  
pp. 1860-1868 ◽  
Author(s):  
Bruno Stuhlmüller ◽  
Ricardo Jerez ◽  
Gert Hausdorf ◽  
Hans-R. Barthel ◽  
Michael Meurer ◽  
...  
Keyword(s):  
Membrane Proteins ◽  
Cell Membrane ◽  
Muscle Cell ◽  
Cell Membrane Proteins ◽  
Muscle Cell Membrane

scholarly journals Spatial targeting of type II protein kinase A to filopodia mediates the regulation of growth cone guidance by cAMP

2007 ◽  
Vol 176 (1) ◽  
pp. 101-111 ◽  
Author(s):  
Jianzhong Han ◽  
Liang Han ◽  
Priyanka Tiwari ◽  
Zhexing Wen ◽  
James Q. Zheng
Keyword(s):  
Protein Kinase ◽  
Protein Kinase A ◽  
Growth Cone ◽  
Regulatory Protein ◽  
Cyclic Adenosine Monophosphate ◽  
Spatial Localization ◽  
Adenosine Monophosphate ◽  
Type Ii ◽  
Regulation Of Growth ◽  
Kinase A

The second messenger cyclic adenosine monophosphate (cAMP) plays a pivotal role in axonal growth and guidance, but its downstream mechanisms remain elusive. In this study, we report that type II protein kinase A (PKA) is highly enriched in growth cone filopodia, and this spatial localization enables the coupling of cAMP signaling to its specific effectors to regulate guidance responses. Disrupting the localization of PKA to filopodia impairs cAMP-mediated growth cone attraction and prevents the switching of repulsive responses to attraction by elevated cAMP. Our data further show that PKA targets protein phosphatase-1 (PP1) through the phosphorylation of a regulatory protein inhibitor-1 (I-1) to promote growth cone attraction. Finally, we find that I-1 and PP1 mediate growth cone repulsion induced by myelin-associated glycoprotein. These findings demonstrate that the spatial localization of type II PKA to growth cone filopodia plays an important role in the regulation of growth cone motility and guidance by cAMP.

scholarly journals Identification of novel therapeutic targets for histone 3 mutated children’s brain tumour, using unique tumour cell surface proteomic signatures

2021 ◽  
Vol 23 (Supplement_4) ◽  
pp. iv9-iv9
Author(s):  
Anya Snary ◽  
Richard Grundy ◽  
Rob Layfield ◽  
Ruman Rahman ◽  
Farhana Haque
Keyword(s):  
Membrane Proteins ◽  
Cell Membrane ◽  
Cell Surface ◽  
Brain Tumours ◽  
Expression Patterns ◽  
Surface Membrane ◽  
Therapeutic Targets ◽  
Molecular Signature ◽  
Histone 3 ◽  
Cell Membrane Proteins

Abstract Aims Improvements in the treatments for childhood and adolescent brain tumours, High-Grade Glioma (pHGG) and Diffuse Intrinsic Pontine Glioblastoma (DIPG), have not advanced much and they continue to carry a very poor prognosis. These brain tumours are now defined by mutations affecting histone 3 proteins, indeed 80% of DIPGs harbour histone H3.1 and H3.3 K27M somatic mutations whilst 30% of pHGGs exhibit H3.3 G34R or G34V mutations. We hypothesized that the histone 3 mutant tumours will have distinct mutation specific surfactome (cell membrane proteins) signature. Method We therefore analysed the cell surface proteomics of pHGG and DIPG, in order to identify novel targets for therapy. We have at first isolated the cell membrane fractions from a range of patient cells carrying different histone 3 mutations (G34R, G34V), relative to wild type histone 3. A comparative quantitative mass-spectrometry analyses of these cell surface membrane fractions is then performed. Results The results obtained to date demonstrated unique differential cell membrane expression patterns which correlated to specific mutation type. For example, increased expression of Ras-related proteins Rab-3, Rab-3D is detected only in histone H3.3-G34R mutated cell line in comparison. Conclusion Identification and analyses of these unique cell membrane proteins’ association with specific in H3.3 mutation in pHGG, will help to identify precise mutation specific therapeutic targets, benefiting the patients to receive therapy based on tumour’s molecular signature.

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