Biochemical Analysis of Lipid Rafts to Study Pathogenic Mechanisms of Neural Diseases

2020 ◽  
pp. 37-46
Author(s):  
Ernesto R. Bongarzone ◽  
Maria I. Givogri
Keyword(s):  
Lipid Rafts ◽  
Biochemical Analysis ◽  
Pathogenic Mechanisms ◽  
Neural Diseases

Mitochondria in Cardiomyopathy: Alterations in Size, Number and Internal Structures

1968 ◽  
Vol 26 ◽  
pp. 126-127
Author(s):  
George Hug ◽  
William K. Schubert
Keyword(s):  
Heart Failure ◽  
Biochemical Analysis ◽  
Left Ventricular ◽  
Size Number ◽  
Internal Structures ◽  
Left Ventricular Outflow ◽  
Chest X Ray ◽  
Myocardial Fibers ◽  
Muscle Biopsies ◽  
Needle Liver Biopsy

A white boy six months of age was hospitalized with respiratory distress and congestive heart failure. Control of the heart failure was achieved but marked cardiomegaly, moderate hepatomegaly, and minimal muscular weakness persisted.At birth a chest x-ray had been taken because of rapid breathing and jaundice and showed the heart to be of normal size. Clinical studies included: EKG which showed biventricular hypertrophy, needle liver biopsy which showed toxic hepatitis, and cardiac catheterization which showed no obstruction to left ventricular outflow. Liver and muscle biopsies revealed no biochemical or histological evidence of type II glycogexiosis (Pompe's disease). At thoracotomy, 14 milligrams of left ventricular muscle were removed. Total phosphorylase activity in the biopsy specimen was normal by biochemical analysis as was the degree of phosphorylase activation. By light microscopy, vacuoles and fine granules were seen in practically all myocardial fibers. The fibers were not hypertrophic. The endocardium was not thickened excluding endocardial fibroelastosis. Based on these findings, the diagnosis of idiopathic non-obstructive cardiomyopathy was made.

3H-galactose and 3H-glucose incorporation into newly synthesized hepatic glycogen in control-fed rats

1986 ◽  
Vol 44 ◽  
pp. 292-293
Author(s):  
J.E. Michaels ◽  
S.A. Garfield ◽  
J.T. Hung ◽  
S.S. Smith ◽  
R.R. Cardell
Keyword(s):  
Biochemical Analysis ◽  
Glycogen Synthesis ◽  
Hepatic Glycogen ◽  
Electron Microscopic ◽  
Once Daily ◽  
Tail Vein ◽  
Tracer Dose ◽  
Glucose Incorporation ◽  
Wet Weight

3H-galactose (gal) and 3H-glucose (glu) were compared to determine which compound was preferable for pulse labeling newly formed hepatic glycogen. Control fed rats were used to achieve substantial and consistent levels of hepatic glycogen and to stimulate glycogen synthesis.Rats fed once daily for 4 hr achieved hepatic glycogen levels > 3% wet weight liver prior to injection by tail vein of a tracer dose of 3H-gal or 3H-glu. The rats were sacrificed 15-120 min later and liver was prepared by routine techniques for light (LM) and electron microscopic (EM) radioautography (RAG) and biochemical analysis.

Caveolin-1, galectin-3 and lipid raft domains in cancer cell signalling

2015 ◽  
Vol 57 ◽  
pp. 189-201 ◽  
Author(s):  
Jay Shankar ◽  
Cecile Boscher ◽  
Ivan R. Nabi
Keyword(s):  
Plasma Membrane ◽  
Lipid Rafts ◽  
Cancer Cell ◽  
Cellular Response ◽  
Spatial Organization ◽  
Essential Feature ◽  
Cell Signalling ◽  
Coated Pits ◽  
Signalling Molecules ◽  
Raft Domains

Spatial organization of the plasma membrane is an essential feature of the cellular response to external stimuli. Receptor organization at the cell surface mediates transmission of extracellular stimuli to intracellular signalling molecules and effectors that impact various cellular processes including cell differentiation, metabolism, growth, migration and apoptosis. Membrane domains include morphologically distinct plasma membrane invaginations such as clathrin-coated pits and caveolae, but also less well-defined domains such as lipid rafts and the galectin lattice. In the present chapter, we will discuss interaction between caveolae, lipid rafts and the galectin lattice in the control of cancer cell signalling.

Spatial control of actin-based motility through plasmalemmal PtdIns(4,5)P2-rich raft assemblies.

2005 ◽  
Vol 72 ◽  
pp. 119-127 ◽  
Author(s):  
Tamara Golub ◽  
Caroni Pico
Keyword(s):  
Protein Kinase ◽  
Cell Surface ◽  
Actin Cytoskeleton ◽  
Lipid Rafts ◽  
Patch Clustering ◽  
Pkc Protein Kinase C ◽  
Membrane Bound ◽  
And Function ◽  
Cytoskeleton Dynamics ◽  
Syndrome Protein

The interactions of cells with their environment involve regulated actin-based motility at defined positions along the cell surface. Sphingolipid- and cholesterol-dependent microdomains (rafts) order proteins at biological membranes, and have been implicated in most signalling processes at the cell surface. Many membrane-bound components that regulate actin cytoskeleton dynamics and cell-surface motility associate with PtdIns(4,5)P2-rich lipid rafts. Although raft integrity is not required for substrate-directed cell spreading, or to initiate signalling for motility, it is a prerequisite for sustained and organized motility. Plasmalemmal rafts redistribute rapidly in response to signals, triggering motility. This process involves the removal of rafts from sites that are not interacting with the substrate, apparently through endocytosis, and a local accumulation at sites of integrin-mediated substrate interactions. PtdIns(4,5)P2-rich lipid rafts can assemble into patches in a process depending on PtdIns(4,5)P2, Cdc42 (cell-division control 42), N-WASP (neural Wiskott-Aldrich syndrome protein) and actin cytoskeleton dynamics. The raft patches are sites of signal-induced actin assembly, and their accumulation locally promotes sustained motility. The patches capture microtubules, which promote patch clustering through PKA (protein kinase A), to steer motility. Raft accumulation at the cell surface, and its coupling to motility are influenced greatly by the expression of intrinsic raft-associated components that associate with the cytosolic leaflet of lipid rafts. Among them, GAP43 (growth-associated protein 43)-like proteins interact with PtdIns(4,5)P2 in a Ca2+/calmodulin and PKC (protein kinase C)-regulated manner, and function as intrinsic determinants of motility and anatomical plasticity. Plasmalemmal PtdIns(4,5)P2-rich raft assemblies thus provide powerful organizational principles for tight spatial and temporal control of signalling in motility.

664: CXCL12/CXCR4 Trans-Activation of HER2 in Lipid Rafts of Prostate Cancer Cell Membranes Promotes Bone Metastasis

2007 ◽  
Vol 177 (4S) ◽  
pp. 223-223
Author(s):  
Sreenivasa R. Chinni ◽  
Hamilto Yamamoto ◽  
Zhong Dong ◽  
Aaron Sabbota ◽  
Sanaa Nabha ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Bone Metastasis ◽  
Lipid Rafts ◽  
Cancer Cell ◽  
Cell Membranes ◽  
Prostate Cancer Cell

173: Lipid Rafts are Negative Regulators of TGFβ Signaling in Ureteral Smooth Muscle Cells

2004 ◽  
Vol 171 (4S) ◽  
pp. 46-46
Author(s):  
Carlos R. Estrada ◽  
Theodora Danciu ◽  
Maximilian Stehr ◽  
Joseph Khoury ◽  
Keith R. Solomon ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Lipid Rafts ◽  
Muscle Cells ◽  
Negative Regulators ◽  
Tgfβ Signaling

63 SAP-97 promotes hKv1.5 compartmentation to lipid rafts and interaction with beta-subunit: consequences on currents properties

2003 ◽  
Vol 2 (1) ◽  
pp. 4
Author(s):  
A MAGUY ◽  
D GODREAU ◽  
P RATAJCZAK ◽  
C HEYMES ◽  
R VRANCKX ◽  
...  
Keyword(s):  
Lipid Rafts ◽  
Beta Subunit

Cerebral sinovenous thrombosis during asparaginase treatment

2003 ◽  
Vol 23 (03) ◽  
pp. 109-112
Author(s):  
A. Hirt ◽  
C. Zwicky ◽  
W.A. Wuillemin ◽  
K. Leibundgut
Keyword(s):  
Acute Lymphoblastic Leukaemia ◽  
Lymphoblastic Leukaemia ◽  
Induction Treatment ◽  
Pathogenic Mechanisms ◽  
Cerebral Sinovenous Thrombosis ◽  
Haemorrhagic Infarction ◽  
Sinovenous Thrombosis

SummaryA boy (age: 71/12 years) with acute lymphoblastic leukaemia developed thrombosis of the sinus sagitalis superior with secondary haemorrhagic infarction while on induction treatment with vincristine, prednisone, and asparaginase. Based on this report, the potential pathogenic mechanisms are discussed with respect to congenital prothrombotic defects as well as to the role of antileukaemic treatment. Current hypotheses on mechanisms for thromboembolism in children and proposed prophylactic strategies are briefly summarized.

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