The structure elucidation and biological activities of high molecular weight algal toxins: maitotoxin, prymnesins and zooxanthellatoxins (1993 to 1999)

2000 ◽  
Vol 17 (3) ◽  
pp. 293-314 ◽  
Author(s):  
Michio Murata ◽  
Takeshi Yasumoto
2021 ◽  
Vol 15 (3) ◽  
pp. 194-201
Author(s):  
Yunze Wang ◽  
Wei Zhang ◽  
Li Ren ◽  
Jing Sun ◽  
Dongbo Zhang

Trimacoside A (1), a new phenylpropanoid glycoside, together with nine known compounds (2−10) was isolated from Tricyrtis maculata. All compounds, except for 8, were firstly isolated from this plant. The structure elucidation of the new compound was carried out by the analysis of spectroscopic data, including 1D, 2D NMR, and HRESIMS. Compounds 1, 4, 5, 7, 8, and 10 showed significant antioxidant activities by DPPH and ABTS assays.


1984 ◽  
Vol 62 (4) ◽  
pp. 203-208 ◽  
Author(s):  
E. Turpin ◽  
J. Wantyghem ◽  
P. Beaudry ◽  
D. Néel ◽  
Y. Goussault

Formaldehyde treatment of Ricinus communis agglutinin, a nonmitogenic toxic 120 000 molecular weight (MW) lectin, yielded two distinct protein fractions: one was heterogeneous and contained high molecular weight lectin polymers (> 120 000), and the other was a homogeneous 120 000 MW protein. Both fractions lost their cytotoxicity after formaldehyde treatment and stimulated thymidine incorporation into lymphocytes. Binding of both treated lectin fractions to lymphocytes exhibited positive cooperativity, whereas binding of untreated lectin did not.


2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Larry S. Sherman ◽  
Steven Matsumoto ◽  
Weiping Su ◽  
Taasin Srivastava ◽  
Stephen A. Back

The glycosaminoglycan hyaluronan (HA), a component of the extracellular matrix, has been implicated in regulating neural differentiation, survival, proliferation, migration, and cell signaling in the mammalian central nervous system (CNS). HA is found throughout the CNS as a constituent of proteoglycans, especially within perineuronal nets that have been implicated in regulating neuronal activity. HA is also found in the white matter where it is diffusely distributed around astrocytes and oligodendrocytes. Insults to the CNS lead to long-term elevation of HA within damaged tissues, which is linked at least in part to increased transcription of HA synthases. HA accumulation is often accompanied by elevated expression of at least some transmembrane HA receptors including CD44. Hyaluronidases that digest high molecular weight HA into smaller fragments are also elevated following CNS insults and can generate HA digestion products that have unique biological activities. A number of studies, for example, suggest that both the removal of high molecular weight HA and the accumulation of hyaluronidase-generated HA digestion products can impact CNS injuries through mechanisms that include the regulation of progenitor cell differentiation and proliferation. These studies, reviewed here, suggest that targeting HA synthesis, catabolism, and signaling are all potential strategies to promote CNS repair.


2011 ◽  
Vol 109 (suppl_1) ◽  
Author(s):  
Jon-Jon R Santiago ◽  
Brian P Bestvater ◽  
Robert R Fandrich ◽  
Elissavet Kardami

Background: High molecular weight, 23 kDa rat FGF-2 (Hi-FGF-2) is composed of an N-terminal extension as well as the 18 kDa core sequence present in low molecular weight (Lo-) FGF-2. Hi- and Lo-FGF-2 have distinct biological activities: unlike Lo-FGF-2, Hi-FGF-2, which is secreted by cardiac non-myocytes, promotes cardiomyocytes hypertrophy in vivo and in vitro . We tested if the paracrine pro-hypertrophic effects of secreted Hi-FGF-2 can be blunted by limited proteolysis of its N-terminal extension. Experimental: Heparin-sepharose-bound Hi-FGF-2 present in rat tissue extracts converted to an approximately 18 kDa protein (*Lo-FGF-2) through truncation of its N-terminal extension, in the absence of protease inhibitors. Serine protease inhibitors such as PMSF fully prevented this conversion. Similarly, purified recombinant rat Hi-FGF-2 was converted to *Lo-FGF-2 by thrombin, a serine protease, and the effect was prevented by hirudin, a thrombin specific inhibitor. Conditioned media from unstimulated or angiotensin II-stimulated rat cardiac non-myocytes (fibroblasts) were used to treat neonatal cardiomyocytes in culture, in the absence or presence of thrombin. Conditioned medium from stimulated (but not unstimulated) cells contained Hi-FGF-2, which promoted cardiomyocyte hypertrophy (increase in cell surface area), and the effect was due to secreted FGF-2 because it was prevented by neutralizing anti-FGF-2 antibodies. Thrombin itself had no effect on cell size but prevented the pro-hypertrophic effect of the conditioned media; while converting the secreted Hi-FGF-2 to *Lo-FGF-2. Conclusions: The truncation of the N-terminal extension of secreted Hi-FGF-2 by serine protease(s) can provide a strategy to prevent undesirable paracrine effects of Hi-FGF-2 (such as cardiac hypertrophy), while maintaining potentially beneficial (cytoprotective, angiogenic) effects associated with Lo-FGF-2.


2016 ◽  
Vol 7 (7) ◽  
pp. 4379-4390 ◽  
Author(s):  
Julien Leclaire ◽  
Guillaume Poisson ◽  
Fabio Ziarelli ◽  
Gerard Pepe ◽  
Frédéric Fotiadu ◽  
...  

A three-dimensional structural model of a complex CO2-based organic framework made from high molecular weight, self-assembled, flexible and multi-functional oligomeric constituents has been determined de novo by solid-state NMR including DNP-enhanced experiments.


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