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71.
72.
α-(Hydroxymethyl)serine was isolated and characterized from the seeds of Vicia pseudo-orobus (Leguminosae). 相似文献
73.
Matthew L. Kraushar Ferdinand Krupp Dermot Harnett Paul Turko Mateusz C. Ambrozkiewicz Thiemo Sprink Koshi Imami Manuel Günnigmann Ulrike Zinnall Carlos H. Vieira-Vieira Theres Schaub Agnieszka Münster-Wandowski Jörg Bürger Ekaterina Borisova Hiroshi Yamamoto Mladen-Roko Rasin Uwe Ohler Dieter Beule Christian M.T. Spahn 《Molecular cell》2021,81(2):304-322.e16
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74.
Hitoshi Suzuki Milan Raska Koshi Yamada Zina Moldoveanu Bruce A. Julian Robert J. Wyatt Yasuhiko Tomino Ali G. Gharavi Jan Novak 《The Journal of biological chemistry》2014,289(8):5330-5339
IgA nephropathy (IgAN), the most common primary glomerulonephritis, is characterized by renal immunodeposits containing IgA1 with galactose-deficient O-glycans (Gd-IgA1). These immunodeposits originate from circulating immune complexes consisting of anti-glycan antibodies bound to Gd-IgA1. As clinical disease onset and activity of IgAN often coincide with mucosal infections and dysregulation of cytokines, we hypothesized that cytokines may affect IgA1 O-glycosylation. We used IgA1-secreting cells derived from the circulation of IgAN patients and healthy controls and assessed whether IgA1 O-glycosylation is altered by cytokines. Of the eight cytokines tested, only IL-6 and, to a lesser degree, IL-4 significantly increased galactose deficiency of IgA1; changes in IgA1 O-glycosylation were robust for the cells from IgAN patients. These cytokines reduced galactosylation of the O-glycan substrate directly via decreased expression of the galactosyltransferase C1GalT1 and, indirectly, via increased expression of the sialyltransferase ST6GalNAc-II, which prevents galactosylation by C1GalT1. These findings were confirmed by siRNA knockdown of the corresponding genes and by in vitro enzyme reactions. In summary, IL-6 and IL-4 accentuated galactose deficiency of IgA1 via coordinated modulation of key glycosyltransferases. These data provide a mechanism explaining increased immune-complex formation and disease exacerbation during mucosal infections in IgAN patients. 相似文献
75.
76.
Kunio Yamada Ryo Norikoshi Katsumi Suzuki Hideo Imanishi Kazuo Ichimura 《Planta》2009,230(6):1115-1127
Petal growth associated with flower opening depends on cell expansion. To understand the role of soluble carbohydrates in
petal cell expansion during flower opening, changes in soluble carbohydrate concentrations in vacuole, cytoplasm and apoplast
of petal cells during flower opening in rose (Rosa hybrida L.) were investigated. We determined the subcellular distribution of soluble carbohydrates by combining nonaqueous fractionation
method and infiltration–centrifugation method. During petal growth, fructose and glucose rapidly accumulated in the vacuole,
reaching a maximum when petals almost reflected. Transmission electron microscopy showed that the volume of vacuole and air
space drastically increased with petal growth. Carbohydrate concentration was calculated for each compartment of the petal
cells and in petals that almost reflected, glucose and fructose concentrations increased to higher than 100 mM in the vacuole.
Osmotic pressure increased in apoplast and symplast during flower opening, and this increase was mainly attributed to increases
in fructose and glucose concentrations. No large difference in osmotic pressure due to soluble carbohydrates was observed
between the apoplast and symplast before flower opening, but total osmotic pressure was much higher in the symplast than in
the apoplast, a difference that was partially attributed to inorganic ions. An increase in osmotic pressure due to the continued
accumulation of glucose and fructose in the symplast may facilitate water influx into cells, contributing to cell expansion
associated with flower opening under conditions where osmotic pressure is higher in the symplast than in the apoplast. 相似文献
77.
Koshi Kunimoto Hisashi Nojima Yuji Yamazaki Toshikazu Yoshikawa Takeshi Okanoue Sachiko Tsukita 《Journal of cellular physiology》2009,220(3):621-631
The spatio‐temporal regulation of hepatocyte proliferation is a critical issue in liver regeneration. Here, in normal and regenerating liver as well as in developing liver, we examined its expression/localization of IQGAP3, which was most recently reported as a Ras/Rac/Cdc42‐binding proliferation factor associated with cell–cell contacts in epithelial‐type cells. In parallel, the expression/localization of Rac/Cdc42‐binding IQGAP1/2 was examined. IQGAP3 showed a specific expression in proliferating hepatocytes positive for the proliferating marker Ki‐67, the levels of expressions of mRNAs and proteins were significantly increased in hepatocytes in liver regeneration and development. In immunofluorescence, IQGAP3 was highly enriched at cell–cell contacts of hepatocytes. IQGAP1 and IQGAP2 were exclusively expressed in Kupffer and sinusoidal endothelial cells, respectively, in normal, regenerating, and developing liver. The expression of IQGAP1, but not of IQGAP2, was increased in CCl4‐induced (but not in partial hepatectomy‐induced) liver regeneration. Exclusive expression/localization of IQGAP3 to hepatocytes in the liver likely reflects the specific involvement of the IQGAP3/Ras/ERK signaling cascade in hepatocyte proliferation in addition to the previously identified signaling pathways, possibly by integrating cell–cell contact‐related proliferating signaling events. On the other hand, the Rac/Cdc42‐binding properties of IQGAP1/2/3 may be related to the distinct modes of remodeling due to the different strategies which induced proliferation of liver cells; partial hepatectomy, CCl4 injury, or embryonic development. Thus, the functional orchestration of Ras and the Ras homologous (Rho) family proteins Rac/Cdc42 likely plays a critical role in liver regeneration and development. J. Cell. Physiol. 220: 621–631, 2009. © 2009 Wiley‐Liss, Inc. 相似文献
78.
Rie Oka Katsuyuki Miura Masaru Sakurai Koshi Nakamura Kunimasa Yagi Susumu Miyamoto Tadashi Moriuchi Hiroshi Mabuchi Junji Koizumi Hideki Nomura Yoshiyu Takeda Akihiro Inazu Atsushi Nohara Masa‐Aki Kawashiri Shinya Nagasawa Junji Kobayashi Masakazu Yamagishi 《Obesity (Silver Spring, Md.)》2010,18(1):153-160
Regional fat distribution rather than overall fat volume has been considered to be important to understanding the link between obesity and metabolic disorders. We aimed to evaluate the independent associations of visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT) with metabolic risk factors in apparently healthy middle‐aged Japanese. Participants were 1,119 men and 854 women aged 38–60 years who were not taking medications for diabetes, hypertension, or dyslipidemia. VAT and SAT were measured by use of computed tomography (CT) scanning. VAT and SAT were significantly and positively correlated with each other in men (r = 0.531, P < 0.001) and women (r = 0.589, P < 0.001). In multiple regression analyses, either measure of abdominal adiposity (VAT or SAT) was positively associated with blood pressure, fasting plasma glucose, and log triglyceride (P < 0.001) and inversely with high‐density lipoprotein (HDL)‐cholesterol (P < 0.001). When VAT and SAT were simultaneously included in the model, the association of VAT with triglycerides was maintained (P < 0.001) but that of SAT was lost. The same was true for HDL‐cholesterol in women. For fasting plasma glucose, the association with VAT was strong (P < 0.001) and the borderline association with SAT was maintained (P = 0.060 in men and P = 0.020 in women). Both VAT and SAT were independently associated with blood pressure (P < 0.001). Further adjustment for anthropometric indices resulted in the independent association only with VAT for all risk factors. In conclusion, impacts of VAT and SAT differed among risk factors. VAT showed dominant impacts on triglyceride concentrations in both genders and on HDL‐cholesterol in women, while SAT also had an independent association with blood pressure. 相似文献
79.
Hiroshi Kawakami Takashi Ebata Koshi Koseki Katsuya Matsumoto Koji Okano Hajime Matsushita 《Nucleosides, nucleotides & nucleic acids》2013,32(9):1673-1682
Abstract The condensation reaction between 2,2-diphenylthio-2,3-dideoxyribose and silylated pyrimidine bases was examined. In the presence of TMSOTf as a catalyst, this reaction proceeded to give the nucleosides in the ratio of α: β = 2:8. Each β-anomer was converted to protected 2′,3′-dideoxynucleosides. 相似文献
80.
Ryo Taguchi Masanobu Yamada Kazuhiko Horiguchi Takuya Tomaru Atsushi Ozawa Nobuyuki Shibusawa Koshi Hashimoto Shuichi Okada Tetsurou Satoh Masatomo Mori 《Biochemical and biophysical research communications》2011,(2):378
Multiple endocrine neoplasia type 1 (MEN1) is a rare autosomal dominantly inherited syndrome characterized by parathyroid, gastro-entero-pancreatic and anterior pituitary tumors. Although the tissue selectivity of tumors in specific endocrine organs is the very essence of MEN1, the mechanisms underlying the tissue-selectivity of tumors remain unknown. The product of the Men1 gene, menin, and mixed lineage leukemia (MLL) have been found to cooperatively regulate p27Kip1/CDKN1B (p27) and p18Ink4C/CDKN2C (p18) genes. However, there are no reports on the tissue distribution of these MEN1-related genes. We investigated the expression of these genes in the endocrine and non-endocrine organs of wild-type, Men1 knockout and MLL knockout mice. Men1 mRNA was expressed at a similar level in endocrine and non-endocrine organs. However, MLL, p27 and p18 mRNAs were predominantly expressed in the endocrine organs. Notably, p27 and MLL mRNAs were expressed in the pituitary gland at levels approximately 12- and 17-fold higher than those in the liver. The heterozygotes of Men1 knockout mice the levels of MLL, p27 and p18 mRNAs did not differ from those in the wild-type mice. In contrast, heterozygotes of MLL knockout mice showed significant reductions in p27 mRNA as well as protein levels in the pituitary and p27 and p18 in the pancreatic islets, but not in the liver. This study demonstrated for the first time the predominant expression MEN1-related genes, particularly MLL and p27, in the endocrine organs, and a tissue-specific haploinsuffiency of MLL, but not menin, may lead to a decrease in levels of p27 and p18 mRNAs in endocrine organs. These findings may provide basic information for understanding the mechanisms of tissue selectivity of the tumorigenesis in patients with MEN1. 相似文献