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Glycosylation is the most frequent PTM and contributes significantly to the function of proteins depending on the type of glycosylation. Especially glycan structures like the glycosaminoglycans are considered to constitute themselves the major function of the glycoconjugate which is therefore termed proteoglycan. Here we review recent views on and novel tools for analysing the proteoglycanome, which are directly related to the type of glycanation under investigation. We define the major function of the proteoglycanome to be its interaction with various proteins in many different (patho-)physiological conditions. This is exemplified by the differential glycosaminoglycan-interactome of healthy versus arthritic patient sera. 相似文献
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Raspor Martin Motyka Václav Ninković Slavica Malbeck Jiří Dobrev Petre I. Zdravković-Korać Snežana Simonović Ana Ćosić Tatjana Cingel Aleksandar Savić Jelena Zahajská Lenka Tadić Vojin Dragićević Ivana Č. 《Journal of Plant Growth Regulation》2021,40(1):37-47
Journal of Plant Growth Regulation - Over the last years, cytokinin deficiency has been studied in a variety of plant species, using transgenic expression of cytokinin oxidase/dehydrogenase genes... 相似文献
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Jianing Fu Julien Zuber Mercedes Martinez Brittany Shonts Aleksandar Obradovic Hui Wang Sai-ping Lau Amy Xia Elizabeth E. Waffarn Kristjana Frangaj Thomas M. Savage Michael T. Simpson Suxiao Yang Xinzheng V. Guo Michelle Miron Takashi Senda Kortney Rogers Adeeb Rahman Megan Sykes 《Cell Stem Cell》2019,24(2):227-239.e8
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Atypical forms of incontinentia pigmenti in male individuals result from mutations of a cytosine tract in exon 10 of NEMO (IKK-gamma) 总被引:10,自引:0,他引:10 下载免费PDF全文
Aradhya S Courtois G Rajkovic A Lewis RA Levy M Israël A Nelson DL 《American journal of human genetics》2001,68(3):765-771
Familial incontinentia pigmenti (IP [MIM 308310]), or Bloch-Sulzberger syndrome, is an X-linked dominant and male-lethal disorder. We recently demonstrated that mutations in NEMO (IKK-gamma), which encodes a critical component of the NF-kappaB signaling pathway, were responsible for IP. Virtually all mutations eliminate the production of NEMO, causing the typical skewing of X inactivation in female individuals and lethality in male individuals, possibly through enhanced sensitivity to apoptosis. Most mutations also give rise to classic signs of IP, but, in this report, we describe two mutations in families with atypical phenotypes. Remarkably, each family included a male individual with unusual signs, including postnatal survival and either immune dysfunction or hematopoietic disturbance. We found two duplication mutations in these families, at a cytosine tract in exon 10 of NEMO, both of which remove the zinc (Zn) finger at the C-terminus of the protein. Two deletion mutations were also identified in the same tract in additional families. However, only the duplication mutations allowed male individuals to survive, and affected female individuals with duplication mutations demonstrated random or slight skewing of X inactivation. Similarly, NF-kappaB activation was diminished in the presence of duplication mutations and was completely absent in cells with deletion mutations. These results strongly indicate that male individuals can also suffer from IP caused by NEMO mutations, and we therefore urge a reevaluation of the diagnostic criteria. 相似文献
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