scholarly journals Sphingoid base in pineapple glucosylceramide suppresses experimental allergy by binding leukocyte mono‐immunoglobulin‐like receptor 3

Author(s):  
Ayumi Takemura ◽  
Nobuaki Ohto ◽  
Hiroshige Kuwahara ◽  
Masashi Mizuno
2013 ◽  
Vol 61 (33) ◽  
pp. 7969-7975 ◽  
Author(s):  
Junki Shimajiri ◽  
Makoto Shiota ◽  
Masashi Hosokawa ◽  
Kazuo Miyashita

2018 ◽  
Vol 41 (5) ◽  
pp. 743-748
Author(s):  
Yukitoshi Nagahara ◽  
Kei Kawakami ◽  
Abudubari Sikandan ◽  
Daiki Yagi ◽  
Ryo Nishikawa ◽  
...  
Keyword(s):  

2020 ◽  
Vol 50 (12) ◽  
pp. 1302-1312
Author(s):  
Graham Roberts ◽  
C. Almqvist ◽  
R. Boyle ◽  
J. Crane ◽  
S.P. Hogan ◽  
...  

1994 ◽  
Vol 57 (7) ◽  
pp. 638-644 ◽  
Author(s):  
RONALD T. RILEY ◽  
KENNETH A. VOSS ◽  
HWAN -SOO YOO ◽  
WENTZEL C.A. GELDERBLOM ◽  
ALFRED H. MERRILL

What are the molecular events that fumonisin-induced porcine pulmonary edema syndrome and equine leucoencephalomalacia have in common? Do these animal diseases relate mechanistically to fumonisin toxicity in laboratory rats? There is considerable data indicating that disruption of sphingolipid metabolism plays an important early role in all of these diseases. In vitro studies have revealed that fumonisins and structurally related Alternaria alternata f. sp. lycopersici-toxin (AAL-toxin) are potent inhibitors of the enzyme sphinganine (sphingosine) N-acyl transferase (ceramide synthase). Soon after cultured cells or animals are exposed to fumonisins there is a dramatic increase in the free sphingoid base, sphinganine, in tissues, serum and/or urine. Also, free sphingosine concentration increases, complex sphingolipid concentration decreases, and sphingoid base degradation products and other lipid products also increase. It is hypothesized that disruption of sphingolipid metabolism is an early molecular event in the onset and progression of cell injury and the diseases associated with consumption of fumonisins. However, the exact mechanisms responsible for the diseases will not be easily revealed since the role of sphingolipids in cellular regulation is very complex and not yet fully understood. While fumonisin B1 is non-genotoxic it is a complete carcinogen in rat liver. Recent studies indicate that fumonisins inhibit hepatocyte proliferation in rat liver. It has been hypothesized that hepatotoxicity and effects on hepatocyte proliferation are critical determinants for fumonisin B1 cancer initiation and promotion. Alternatively, recent studies have found that fumonisin B1 has mitogenic activity in cultured fibroblasts. It is conceivable that the mitogenic, cytostatic and cytotoxic potential of fumonisin may all contribute to the animal diseases including liver cancer in rats.


2012 ◽  
Vol 441 (3) ◽  
pp. 789-802 ◽  
Author(s):  
Thomas D. Mullen ◽  
Yusuf A. Hannun ◽  
Lina M. Obeid

Sphingolipid metabolism in metazoan cells consists of a complex interconnected web of numerous enzymes, metabolites and modes of regulation. At the centre of sphingolipid metabolism reside CerSs (ceramide synthases), a group of enzymes that catalyse the formation of ceramides from sphingoid base and acyl-CoA substrates. From a metabolic perspective, these enzymes occupy a unique niche in that they simultaneously regulate de novo sphingolipid synthesis and the recycling of free sphingosine produced from the degradation of pre-formed sphingolipids (salvage pathway). Six mammalian CerSs (CerS1–CerS6) have been identified. Unique characteristics have been described for each of these enzymes, but perhaps the most notable is the ability of individual CerS isoforms to produce ceramides with characteristic acyl-chain distributions. Through this control of acyl-chain length and perhaps in a compartment-specific manner, CerSs appear to regulate multiple aspects of sphingolipid-mediated cell and organismal biology. In the present review, we discuss the function of CerSs as critical regulators of sphingolipid metabolism, highlight their unique characteristics and explore the emerging roles of CerSs in regulating programmed cell death, cancer and many other aspects of biology.


2020 ◽  
Vol 34 (2) ◽  
pp. 3318-3335 ◽  
Author(s):  
Keisuke Jojima ◽  
Mai Edagawa ◽  
Megumi Sawai ◽  
Yusuke Ohno ◽  
Akio Kihara

2002 ◽  
Vol 22 (3) ◽  
pp. 927-934 ◽  
Author(s):  
Michael E. Young ◽  
Tatiana S. Karpova ◽  
Britta Brügger ◽  
Darcy M. Moschenross ◽  
Georgeann K. Wang ◽  
...  

ABSTRACT We have discovered a novel cortical patch structure in Saccharomyces cerevisiae defined by a family of integral plasma membrane proteins, including Sur7p, Ynl194p, and Ydl222p. Sur7p-family patches localized as cortical patches that were immobile and stable. These patches were polarized to regions of the cell with a mature cell wall; they were absent from small buds and the tips of many medium-sized buds. These patches were distinct from other known cortical structures. Digestion of the cell wall caused Sur7p patches to disassemble, indicating that Sur7p requires cell wall-dependent extracellular interactions for its localization as patches. sur7Δ, ydl222Δ, and ynl194Δ mutants had reduced sporulation efficiencies. SUR7 was originally described as a multicopy suppressor of rvs167, whose product is an actin patch component. This suppression is probably mediated by sphingolipids, since deletion of SUR7, YDL222, and YNL194 altered the sphingolipid content of the yeast plasma membrane, and other SUR genes suppress rvs167 via effects on sphingolipid synthesis. In particular, the sphingoid base length and number of hydroxyl groups in inositolphosphorylceramides were altered in sur7Δ, ydl222Δ, and yne194Δ strains.


Sign in / Sign up

Export Citation Format

Share Document