نتایج جستجو برای: beta neurotoxin

تعداد نتایج: 191444  

Journal: :Diabetes 2001
D Bosco C Gonelle-Gispert C B Wollheim P A Halban D G Rouiller

Rat islet beta-cells spread in response to glucose when attached on the matrix produced by a rat bladder carcinoma cell line (804G). Furthermore, in a mixed population of cells, it has been observed previously that spread cells secrete more insulin acutely in response to glucose, compared with cells that remain rounded. These results suggest bi-directional signaling between the islet beta-cell ...

Journal: :The Journal of biological chemistry 1990
R H Fogh W R Kem R S Norton

The three-dimensional structure of the sea anemone polypeptide Stichodactyla helianthus neurotoxin I in aqueous solution has been determined using distance geometry and restrained molecular dynamics simulations based on NMR data acquired at 500 MHz. A set of 470 nuclear Overhauser enhancement values was measured, of which 216 were used as distance restraints in the structure determination along...

M Kamalinejad, M Rezaii, M Roghani, S Nasri, SA Ziaii,

Background: Parkinson’s disease (PD.) is one of the most common neurodegenerative disorders. There are many documents about the effects of oxidative stress on PD. progress. Angiotensin II activates NADPH depending on oxidases and these oxidases produce superoxides. Cerasus avium extract is an angiotensin converting enzyme )ACE( inhibitor in Invitro. Objective: Evaluation of neuroprotective eff...

Journal: :Structure 1997
J C Eads D Ozturk T B Wexler C Grubmeyer J C Sacchettini

BACKGROUND Quinolinic acid (QA) is a neurotoxin and has been shown to be present at high levels in the central nervous system of patients with certain diseases, such as AIDS and meningitis. The enzyme quinolinic acid phosphoribosyltransferase (QAPRTase) provides the only route for QA metabolism and is also an essential step in de novo NAD biosynthesis. QAPRTase catalyzes the synthesis of nicoti...

Journal: :Microbiological Reviews 1980

2013
Yeping Ruan Li Yao Bingbing Zhang Shuijuan Zhang Jianyou Guo

BACKGROUND Neurotoxin-Nna (NT), an analgesic peptide separated from the venom of Naja naja atra, has reported to have an exceptional specificity to block transmission of the nerve impulse by binding to the α- subunit of the nicotinic acetylcholine receptor in the membrane. However, little information is available on the anti-inflammatory effects of NT. Therefore, the anti-inflammatory activity ...

Journal: :Archives of biochemistry and biophysics 1985
J J Schmidt V Sathyamoorthy B R DasGupta

Clostridium botulinum type E neurotoxin, a single-chain protein of Mr 147,000, was purified and subjected to amino acid sequencing. The same was done for single-chain botulinum type B neurotoxin (Mr 152,000), and for the heavy and light chains (Mr 104,000 and 51,000 respectively) derived from type B by limited trypsin digestion. Twelve to eighteen residues were identified and the following conc...

2005
Joseph W. Arndt Jenny Gu Lukasz Jaroszewski Robert Schwarzenbacher Michael A. Hanson Frank J. Lebeda Raymond C. Stevens

0022-2836/$ see front matter q 2004 E Present address: J. Gu, San Diego Center, University of California San Drive, La Jolla, CA 92093, USA. Abbreviations used: HA, hemagg non-toxic non-hemagglutinin; BoNT neurotoxin; NAP, neurotoxin-associ root-mean-square deviation; TeNT, E-mail address of the correspond [email protected] The hemagglutinating protein HA33 from Clostridium botulinum is assoc...

Journal: :The Biochemical journal 1997
F Tonello G Schiavo C Montecucco

Tetanus neurotoxin was depleted of its catalytic Zn2+ ion, and the apotoxin was reconstituted with different transition metal ions. The Mn2+- and Co2+-tetanus neurotoxins are highly active in the proteolysis of vesicle-associated membrane protein/synaptobrevin, the natural substrate of this toxin, whereas Cu2+ and Fe2+ minimally supported proteolytic activity. The visible absorbance spectrum of...

2012
Zhongxing Peng Chen J. Glenn Morris Ramon L. Rodriguez Aparna Wagle Shukla John Tapia-Núñez Michael S. Okun

BACKGROUND Two decades ago, botulinum neurotoxin (BoNT) type A was introduced to the commercial market. Subsequently, the toxin was approved by the FDA to address several neurological syndromes, involving muscle, nerve, and gland hyperactivity. These syndromes have typically been associated with abnormalities in cholinergic transmission. Despite the multiplicity of botulinal serotypes (designat...

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