Faculty Opinions recommendation of A Subsidiary Cell-Localized Glucose Transporter Promotes Stomatal Conductance and Photosynthesis.

Author(s):  
Julian Schroeder ◽  
Paulo Ceciliato
2019 ◽  
Vol 31 (6) ◽  
pp. 1328-1343 ◽  
Author(s):  
Hai Wang ◽  
Shijuan Yan ◽  
Hongjia Xin ◽  
Wenjie Huang ◽  
Hao Zhang ◽  
...  

2013 ◽  
Vol 83 (3) ◽  
pp. 188-197 ◽  
Author(s):  
Rebecca L. Sweet ◽  
Jason A. Zastre

It is well established that thiamine deficiency results in an excess of metabolic intermediates such as lactate and pyruvate, which is likely due to insufficient levels of cofactor for the function of thiamine-dependent enzymes. When in excess, both pyruvate and lactate can increase the stabilization of the hypoxia-inducible factor 1-alpha (HIF-1α) transcription factor, resulting in the trans-activation of HIF-1α regulated genes independent of low oxygen, termed pseudo-hypoxia. Therefore, the resulting dysfunction in cellular metabolism and accumulation of pyruvate and lactate during thiamine deficiency may facilitate a pseudo-hypoxic state. In order to investigate the possibility of a transcriptional relationship between hypoxia and thiamine deficiency, we measured alterations in metabolic intermediates, HIF-1α stabilization, and gene expression. We found an increase in intracellular pyruvate and extracellular lactate levels after thiamine deficiency exposure to the neuroblastoma cell line SK-N-BE. Similar to cells exposed to hypoxia, there was a corresponding increase in HIF-1α stabilization and activation of target gene expression during thiamine deficiency, including glucose transporter-1 (GLUT1), vascular endothelial growth factor (VEGF), and aldolase A. Both hypoxia and thiamine deficiency exposure resulted in an increase in the expression of the thiamine transporter SLC19A3. These results indicate thiamine deficiency induces HIF-1α-mediated gene expression similar to that observed in hypoxic stress, and may provide evidence for a central transcriptional response associated with the clinical manifestations of thiamine deficiency.


2013 ◽  
Vol 51 (01) ◽  
Author(s):  
A Koch ◽  
P Wild ◽  
M Kreutz ◽  
A Bosserhoff ◽  
C Hellerbrand

Author(s):  
Hasan Akduman ◽  
Dilek Dilli ◽  
Serdar Ceylaner

AbstractCongenital glucose-galactose malabsorption (CGGM) is an autosomal recessive disorder originating from an abnormal transporter mechanism in the intestines. It was sourced from a mutation in the SLC5A1 gene, which encodes a sodium-dependent glucose transporter. Here we report a 2-day-old girl with CGGM who presented with severe hypernatremic dehydration due to diarrhea beginning in the first hours of life. Mutation analysis revealed a novel homozygous mutation NM_000343.3 c.127G > A (p.Gly43Arg) in the SLC5A1 gene. Since CGGM can cause fatal diarrhea in the early neonatal period, timely diagnosis of the disease seems to be essential.


Diabetes ◽  
1987 ◽  
Vol 36 (4) ◽  
pp. 546-549 ◽  
Author(s):  
T. B. Shows ◽  
R. L. Eddy ◽  
M. G. Byers ◽  
Y. Fukushima ◽  
C. R. Dehaven ◽  
...  

Diabetes ◽  
1991 ◽  
Vol 40 (2) ◽  
pp. 275-279 ◽  
Author(s):  
S. A. Wake ◽  
J. A. Sowden ◽  
L. H. Storlien ◽  
D. E. James ◽  
P. W. Clark ◽  
...  

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