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Articles by M Yu
Total Records ( 5 ) for M Yu
  G Hong , S Jiang , M Yu , Y Yang , F Li , F Xue and Z. Wei
 

The complete mitochondrial genome (mitogenome) of Artogeia melete was determined as being composed of 15,140 bp, including 13 protein-coding genes (PCGs), 2 rRNA genes, 22 tRNA genes, and one control region. The gene order of A. melete mitogenome is typical of Lepidoptera and differs from the insect ancestral type in the location of trnM. The A. melete mitogenome has a total of 119 bp of intergenic spacer sequences spread over 10 regions, ranging in sizes between 1 and 48 bp. The nucleotide composition of the A. melete mitogenome is also biased toward A + T nucleotides (79.77%), which is higher than that of Ochrogaster lunifer (77.84%), but lower than nine other lepidopterans sequenced. The PCGs have typical mitochondrial start codons, except for cox1, which contains the unusual CGA. The cox1, cox2, nad2, and nad5 genes of the A. melete mitogenome have incomplete stop codons (T). The A. melete A + T-rich region contains some conserved structures that are similar to those found in other lepidopteran mitogenomes, including a structure combining the motif ‘ATAGA’, a 19-bp poly(T) stretch, a microsatellite (AT)n element, and a 9-bp poly(A) upstream trnM. The A. melete mitogenome contains a duplicated 36-bp repeat element, which consists of a 26-bp core sequence flanked by 10-bp perfectly inverted repeats.

  X Pan , N Gong , J Zhao , Z Yu , F Gu , J Chen , X Sun , L Zhao , M Yu , Z Xu , W Dong , Y Qin , G Fei , C Zhong and T. L. Xu
 

Reduction of glucose metabolism in brain is one of the main features of Alzheimer’s disease. Thiamine (vitamin B1)-dependent processes are critical in glucose metabolism and have been found to be impaired in brains from patients with Alzheimer’s disease. However, thiamine treatment exerts little beneficial effect in these patients. Here, we tested the effect of benfotiamine, a thiamine derivative with better bioavailability than thiamine, on cognitive impairment and pathology alterations in a mouse model of Alzheimer’s disease, the amyloid precursor protein/presenilin-1 transgenic mouse. We show that after a chronic 8 week treatment, benfotiamine dose-dependently enhanced the spatial memory of amyloid precursor protein/presenilin-1 mice in the Morris water maze test. Furthermore, benfotiamine effectively reduced both amyloid plaque numbers and phosphorylated tau levels in cortical areas of the transgenic mice brains. Unexpectedly, these effects were not mimicked by another lipophilic thiamine derivative, fursultiamine, although both benfotiamine and fursultiamine were effective in increasing the levels of free thiamine in the brain. Most notably, benfotiamine, but not fursultiamine, significantly elevated the phosphorylation level of glycogen synthase kinase-3 and -3β, and reduced their enzymatic activities in the amyloid precursor protein/presenilin-1 transgenic brain. Therefore, in the animal Alzheimer’s disease model, benfotiamine appears to improve the cognitive function and reduce amyloid deposition via thiamine-independent mechanisms, which are likely to include the suppression of glycogen synthase kinase-3 activities. These results suggest that, unlike many other thiamine-related drugs, benfotiamine may be beneficial for clinical Alzheimer’s disease treatment.

  M Yu , G. A Smolen , J Zhang , B Wittner , B. J Schott , E Brachtel , S Ramaswamy , S Maheswaran and D. A. Haber
 

Epithelial-to-mesenchymal transition (EMT) plays an important role during normal embryogenesis, and it has been implicated in cancer invasion and metastasis. Here, we report that Ladybird homeobox 1 (LBX1), a developmentally regulated homeobox gene, directs expression of the known EMT inducers ZEB1, ZEB2, Snail1, and transforming growth factor β2 (TGFB2). In mammary epithelial cells, overexpression of LBX1 leads to morphological transformation, expression of mesenchymal markers, enhanced cell migration, increased CD44high/CD24low progenitor cell population, and tumorigenic cooperation with known oncogenes. In human breast cancer, LBX1 is up-regulated in the unfavorable estrogen receptor (ER)/progesterone (PR)/HER2 triple-negative basal-like subtype. Thus, aberrant expression of LBX1 may lead to the activation of a developmentally regulated EMT pathway in human breast cancer.

  G. A Smolen , J Zhang , M. J Zubrowski , E. J Edelman , B Luo , M Yu , L. W Ng , C. M Scherber , B. J Schott , S Ramaswamy , D Irimia , D. E Root and D. A. Haber
 

To define the functional pathways regulating epithelial cell migration, we performed a genome-wide RNAi screen using 55,000 pooled lentiviral shRNAs targeting ~11,000 genes, selecting for transduced cells with increased motility. A stringent validation protocol generated a set of 31 genes representing diverse pathways whose knockdown dramatically enhances cellular migration. Some of these pathways share features of epithelial-to-mesenchymal transition (EMT), and together they implicate key regulators of transcription, cellular signaling, and metabolism, as well as novel modulators of cellular trafficking, such as DLG5. In delineating downstream pathways mediating these migration phenotypes, we observed universal activation of ERKs and a profound dependence on their RSK effectors. Pharmacological inhibition of RSK dramatically suppresses epithelial cell migration induced by knockdown of all 31 genes, suggesting that convergence of diverse migratory pathways on this kinase may provide a therapeutic opportunity in disorders of cell migration, including cancer metastasis.

  G Fu , Y Chen , M Yu , A Podd , J Schuman , Y He , L Di , M Yassai , D Haribhai , P. E North , J Gorski , C. B Williams , D Wang and R. Wen
 

Phospholipase C1 (PLC1) is an important signaling effector of T cell receptor (TCR). To investigate the role of PLC1 in T cell biology, we generated and examined mice with T cell–specific deletion of PLC1. We demonstrate that PLC1 deficiency affects positive and negative selection, significantly reduces single-positive thymocytes and peripheral T cells, and impairs TCR-induced proliferation and cytokine production, and the activation of ERK, JNK, AP-1, NFAT, and NF-B. Importantly, PLC1 deficiency impairs the development and function of FoxP3+ regulatory T cells, causing inflammatory/autoimmune symptoms. Therefore, PLC1 is essential for T cell development, activation, and tolerance.

 
 
 
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