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  • 1
    ISSN: 1432-2242
    Keywords: Rice (Oryza sativa L.) ; Seed protein loci ; Codominance ; Inheritance ; SDS-PAGE
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary Previous studies indicated two types of phenotypic protein markers as two minor bands of SDS-PAGE for rice storage protein. A variant derived from a Pakistani variety, Dular, was found to show a mobility variant with Band 11, a relatively faster-moving band as compared to Band 10, while most of the other cultivated rices exhibited Band 10 at a molecular weight of around 100–110 K. Band 11 was also observed in several wild rice species. How this variant occurred is not known. Another marker is characterized by the presence of either Band 56 (slower-migrating band) or Band 57 (faster-migrating band) in most cultivars at a molecular weight of about 28–27 K. Most indica varieties developed in Taiwan have Band 57 and japonica varieties have Band 56. Genetic analysis of F1, F2 and F3 seeds from interstrain crosses indicated that Band 10 versus Band 11 and Band 56 versus Band 57 are due to codominant alleles at two loci. Tests of independent inheritance between these two loci (Band 10/11 versus Band 56/57) indicated that there is no linkage between them. Both of these two protein loci encode for endosperm proteins and mostly belong to the minor polypeptide subunits of the glutelin fraction of rice seed proteins. Studies on reciprocal crosses indicate dosage effects as exhibited in band patterns. Variations in band intensity were frequently observed when the maternal genotype was different.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    [s.l.] : Macmillian Magazines Ltd.
    Nature 402 (1999), S. 42-46 
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] The first fossil chordates are found in deposits from the Cambrian period (545–490 million years ago), but their earliest record is exceptionally sporadic and is often controversial. Accordingly, it has been difficult to construct a coherent phylogenetic synthesis for the basal chordates. ...
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1572-9540
    Source: Springer Online Journal Archives 1860-2000
    Topics: Physics
    Notes: Abstract The rapidly queoching samples of Sm20Fe70Ti10 were prepared by melt spinning. The coercivities of crystallized ribbons were found to vary with the spinning velocity. The value of coercivity obtained was 3.2kOe, which is higher than that reached in Sm−Fe−Ti alloys with the ThMn17 structure. The results of Mössbauer effect and X ray diffraction analyses indicate that the alloy consists of SmFe2, SmFe3, an undetermined paramagnetic phase and the minor phase of Sm2Fe17.
    Type of Medium: Electronic Resource
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  • 4
    Publication Date: 2018-10-26
    Description: Acute myeloid leukemia (AML) can evade the mouse and human innate immune system by suppressing natural killer (NK) cell development and NK cell function. This is driven in part by the overexpression of microRNA (miR)–29b in the NK cells of AML patients, but how this occurs is unknown. In the current study, we demonstrate that the transcription factor aryl hydrocarbon receptor (AHR) directly regulates miR-29b expression. We show that human AML blasts activate the AHR pathway and induce miR-29b expression in NK cells, thereby impairing NK cell maturation and NK cell function, which can be reversed by treating NK cells with an AHR antagonist. Finally, we show that inhibition of constitutive AHR activation in AML blasts lowers their threshold for apoptosis and decreases their resistance to NK cell cytotoxicity. Together, these results identify the AHR pathway as a molecular mechanism by which AML impairs NK cell development and function. The results lay the groundwork in establishing AHR antagonists as potential therapeutic agents for clinical development in the treatment of AML.
    Keywords: Immunobiology and Immunotherapy, Myeloid Neoplasia
    Print ISSN: 0006-4971
    Electronic ISSN: 1528-0020
    Topics: Biology , Medicine
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  • 5
    Publication Date: 2018-02-14
    Description: The genotype II.4 (GII.4) variants of human noroviruses (HuNVs) are recognized as the major agent of global gastroenteritis outbreaks. Due to the lack of an efficient cell culture system for HuNV propagation, the exact roles of HuNV-encoded nonstructural proteins (including Nterm, NTPase, P22, VPg, Pro, and RdRp) in viral replication or pathogenesis have not yet been fully understood. Here, we report the molecular characterization of the GII.4 HuNV-encoded NTPase (designated GII-NTPase). Results from our studies showed that GII-NTPase forms vesicular or nonvesicular textures in the cell cytoplasm, and the nonvesicular fraction of GII-NTPase significantly localizes to the endoplasmic reticulum (ER) or mitochondria. Deletion analysis revealed that the N-terminal 179-amino-acid (aa) region of GII-NTPase is required for vesicle formation and for ER colocalization, whereas the C-terminal region is involved in mitochondrial colocalization. In particular, two mitochondrion-targeting domains were identified in the C-terminal region of GII-NTPase which perfectly colocalized with mitochondria when the N-terminal region of GII-NTPase was deleted. However, the corresponding C-terminal portions of NTPase derived from the GI HuNV did not show mitochondrial colocalization. We also found that GII-NTPase physically interacts with itself as well as with Nterm and P22, but not VPg, Pro, and RdRp, in cells. The Nterm- and P22-interacting region was mapped to the N-terminal 179-aa region of GII-NTPase, whereas the self-assembly of GII-NTPase could be achieved via a head-to-head, tail-to-tail, or head-to-tail configuration. More importantly, we demonstrate that GII-NTPase possesses a proapoptotic activity, which can be further enhanced by coexpression with Nterm or P22. IMPORTANCE Despite the importance of human norovirus GII.4 variants in global gastroenteritis outbreaks, the basic biological functions of the viral nonstructural proteins in cells remain rarely investigated. In this report, we focus our studies on characteristics of the GII.4 norovirus-encoded NTPase (GII-NTPase). We unexpectedly find that GII-NTPase can perfectly colocalize with mitochondria after its N-terminal region is deleted. However, such a phenomenon is not observed for NTPase encoded by a GI strain. We further reveal that the N-terminal 179-aa region of GII-NTPase is sufficient to mediate (i) vesicle formation, (ii) ER colocalization, (iii) the interaction with two other nonstructural proteins, including Nterm and P22, (iv) the formation of homodimers or homo-oligomers, and (v) the induction of cell apoptosis. Taken together, our findings emphasize that the virus-encoded NTPase must have multiple activities during viral replication or pathogenesis; however, these activities may vary somewhat among different genogroups.
    Print ISSN: 0022-538X
    Electronic ISSN: 1098-5514
    Topics: Medicine
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  • 6
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    German Medical Science GMS Publishing House; Düsseldorf
    In:  Deutscher Kongress für Orthopädie und Unfallchirurgie (DKOU 2017); 20171024-20171027; Berlin; DOCIN33-296 /20171023/
    Publication Date: 2017-10-23
    Keywords: Total hip arthroplasty ; intra-operative acetabular fracture ; classification ; treatment ; ddc: 610
    Language: English
    Type: conferenceObject
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  • 7
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    German Medical Science GMS Publishing House; Düsseldorf
    In:  Deutscher Kongress für Orthopädie und Unfallchirurgie (DKOU 2017); 20171024-20171027; Berlin; DOCIN12-1194 /20171023/
    Publication Date: 2017-10-23
    Keywords: T1rho/T2 mapping ; osteonecrosis ; cartilage denaturalization ; ARCO stage ; ddc: 610
    Language: English
    Type: conferenceObject
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  • 8
    Keywords: MUTATIONS ; CRYSTAL-STRUCTURE ; IMMUNE DYSREGULATION ; POLYENDOCRINOPATHY ; TARGET GENES ; TUMOR-SUPPRESSOR P53 ; TRANSCRIPTION FACTOR FOXP3 ; ENTEROPATHY ; NFAT ; IPEX
    Abstract: The transcription factor FOXP3 is essential for the suppressive function of regulatory T cells that are required for maintaining self-tolerance. We have solved the crystal structure of the FOXP3 forkhead domain as a ternary complex with the DNA-binding domain of the transcription factor NFAT1 and a DNA oligonucleotide from the interleukin-2 promoter. A striking feature of this structure is that FOXP3 forms a domain-swapped dimer that bridges two molecules of DNA. Structure-guided or autoimmune disease (IPEX)-associated mutations in the domain-swap interface diminished dimer formation by the FOXP3 forkhead domain without compromising FOXP3 DNA binding. These mutations also eliminated T cell-suppressive activity conferred by FOXP3, both in vitro and in a murine model of autoimmune diabetes in vivo. We conclude that FOXP3-mediated suppressor function requires dimerization through the forkhead domain and that mutations in the dimer interface can lead to the systemic autoimmunity observed in IPEX patients.
    Type of Publication: Journal article published
    PubMed ID: 21458306
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  • 9
    Keywords: CELL-LINE ; BLOOD-PRESSURE ; KNOCKOUT MICE ; STEROID-HORMONE RECEPTORS ; aldosterone ; HISTONE METHYLATION ; EPITHELIAL SODIUM-CHANNEL ; MEDULLARY COLLECTING DUCT ; NA+ CHANNEL ; FUSION PARTNER
    Abstract: Aldosterone is a major regulator of Na(+) absorption and acts by activating the mineralocorticoid receptor (MR) to stimulate the epithelial Na(+) channel (ENaC). MR(-/-) mice exhibited pseudohypoaldosteronism type 1 (hyponatremia, hyperkalemia, salt wasting, and high levels of aldosterone) and died around postnatal day 10. However, if and how MR regulates ENaC transcription remain incompletely understood. Our earlier work demonstrated that aldosterone activates alphaENaC transcription by reducing expression of Dot1a and Af9 and by impairing Dot1a-Af9 interaction. Most recently, we reported identification of a major Af9 binding site in the alphaENaC promoter and upregulation of alphaENaC mRNA expression in mouse kidneys lacking Dot1a. Despite these findings, the putative antagonism between the MR/aldosterone and Dot1a-Af9 complexes has never been addressed. The molecular defects leading to PHA-1 in MR(-/-) mice remain elusive. Here, we report that MR competes with Dot1a to bind Af9. MR/aldosterone and Dot1a-Af9 complexes mutually counterbalance ENaC mRNA expression in inner medullary collecting duct 3 (IMCD3) cells. Real-time RT-quantitative PCR revealed that 5-day-old MR(-/-) vs. MR(+/+) mice had significantly lower alphaENaC mRNA levels. This change was associated with an increased Af9 binding and H3 K79 hypermethylation in the alphaENaC promoter. Therefore, this study identified MR as a novel binding partner and regulator of Af9 and a novel mechanism coupling MR-mediated activation with relief of Dot1a-Af9-mediated repression via MR-Af9 interaction. Impaired ENaC expression due to failure to inhibit Dot1a-Af9 may play an important role in the early stages of PHA-1 (before postnatal day 8) in MR(-/-) mice.
    Type of Publication: Journal article published
    PubMed ID: 24026182
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  • 10
    Keywords: CELLS ; THERAPY ; DIFFERENTIATION ; MICE ; CHILDREN ; MYCN ; 13-CIS-RETINOIC ACID ; INHIBITORS ; senescence ; HIGH-RISK NEUROBLASTOMA
    Abstract: Neuroblastoma is an embryonal malignancy of the developing neural crest. Despite improvements in treatment, prognoses remain dire for patients with high-risk disease. Interest in this enigmatic cancer has led to a rapidly changing research landscape and we report on the recent advances in four themes that were discussed at the 3rd Neuroblastoma Research Symposium: (1) The epigenetic signature of neuroblastoma and the epigenetic control of tumour development, (2) novel approaches to targeting MYCN, (3) valuable in vivo modelling and (4) improving differentiation therapies based on a knowledge of normal sympathetic neuron development. Through lively discussion, the development of combined therapies with synergistic effects for which we have a good mechanistic understanding emerged as offering greatest promise. Drug synergies enhance efficacy but also specificity, the latter crucial for reducing long-term side effects in young children.
    Type of Publication: Journal article published
    PubMed ID: 24803179
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