排序方式: 共有9条查询结果,搜索用时 187 毫秒
1
1.
Hessa T Meindl-Beinker NM Bernsel A Kim H Sato Y Lerch-Bader M Nilsson I White SH von Heijne G 《Nature》2007,450(7172):1026-1030
2.
Gout AM;ADPKD Gene Variant Consortium Ravine D Harris PC Rossetti S Peters D Breuning M Henske EP Koizumi A Inoue S Shimizu Y Thongnoppakhun W Yenchitsomanus PT Deltas C Sandford R Torra R Turco AE Jeffery S Fontes M Somlo S Furu LM Smulders YM Mercier B Ferec C Burtey S Pei Y Kalaydjieva L Bogdanova N McCluskey M Geon LJ Wouters CH Reiterova J Stekrová J San Millan JL Aguiari G Del Senno L 《Nature genetics》2007,39(4):427-428
3.
Hoogenraad CC Koekkoek B Akhmanova A Krugers H Dortland B Miedema M van Alphen A Kistler WM Jaegle M Koutsourakis M Van Camp N Verhoye M van der Linden A Kaverina I Grosveld F De Zeeuw CI Galjart N 《Nature genetics》2002,32(1):116-127
Williams syndrome is a neurodevelopmental disorder caused by the hemizygous deletion of 1.6 Mb on human chromosome 7q11.23. This region comprises the gene CYLN2, encoding CLIP-115, a microtubule-binding protein of 115 kD. Using a gene-targeting approach, we provide evidence that mice with haploinsufficiency for Cyln2 have features reminiscent of Williams syndrome, including mild growth deficiency, brain abnormalities, hippocampal dysfunction and particular deficits in motor coordination. Absence of CLIP-115 also leads to increased levels of CLIP-170 (a closely related cytoplasmic linker protein) and dynactin at the tips of growing microtubules. This protein redistribution may affect dynein motor regulation and, together with the loss of CLIP-115-specific functions, underlie neurological alterations in Williams syndrome. 相似文献
4.
Stephan Fricke Nadja Hilger Christian Fricke Uta Schönfelder Gerhard Behre Peter Ruschpler Andreas Boldt Christopher Oelkrug Ulrich Sack Frank Emmrich 《Cellular and molecular life sciences : CMLS》2014,71(11):2135-2148
This is the first report showing that an epitope-specific ex vivo modulation of an allogeneic hematopoietic stem cell graft by the anti-human CD4 antibody MAX.16H5 IgG1 simultaneously facilitates the anti-tumor capacity of the graft (Graft-versus-leukemia effect, GvL) and the long-term suppression of the deleterious side effect Graft-versus-host-disease (GvHD). To distinguish and consolidate GvL from GvHD, the anti-human CD4 antibody MAX16.H5 IgG1 was tested in murine GvHD and tumor models. The survival rate was significantly increased in recipients receiving a MAX.16H5 IgG1 short-term (2 h) pre-incubated graft even when tumor cells were co-transplanted or when recipient mice were treated by MAX.16H5 IgG1 before transplantation. After engraftment, regulatory T-cells are generated only supporting the GvL effect. It was also possible to transfer the immune tolerance from GvHD-free recipient chimeras into third party recipient mice without the need of reapplication of MAX.16H5 IgG1 anti-human CD4 antibodies. These findings are also benefical for patients with leukemia when no matched related or unrelated donor is available and provides a safer allogeneic HSCT, which is more effective against leukemia. It also facilitates allogeneic (stem) cell transplantations for other indications (e.g., autoimmune-disorders). 相似文献
5.
Neumeister B Faigle M Spitznagel D Mainka A Ograbek A Wieland H Mannowetz N Rammensee HG 《Cellular and molecular life sciences : CMLS》2005,62(5):578-588
Legionella (L.) pneumophila, the causative agent of Legionnaires disease, is an intracellular pathogen of alveolar macrophages that resides in a compartment displaying features of endoplasmatic reticulum (ER). In this study, we show that intracellular multiplication of L. pneumophila results in a remarkable decrease in MHC class I expression by the infected monocytes. During intracellular multiplication, L. pneumophila absorbs ER-resident chaperons such as calnexin and BiP, molecules that are required for the correct formation of the MHC class I complex. Due to reduced MHC class I expression, stimulation of allogeneic blood mononuclear cells was severely inhibited by infected host cells but cytotoxicity of autologous natural killer cells against Legionella-infected monocytes was not enhanced. Thus, reduced expression of MHC class I in infected monocytes may resemble a new immune escape mechanism induced by L. pneumophila.Received 22 November 2004; received after revision 27 December 2004; accepted 5 January 2005 相似文献
6.
Characterization of murine non-adherent bone marrow cells leading to recovery of endogenous hematopoiesis 总被引:1,自引:1,他引:0
Stephan Fricke Christian Fricke Christopher Oelkrug Nadja Hilger Uta Sch?nfelder Manja Kamprad J?rg Lehmann Johannes Boltze Frank Emmrich Ulrich Sack 《Cellular and molecular life sciences : CMLS》2010,67(23):4095-4106
Non-adherent bone marrow-derived cells (NA-BMCs) are a mixed cell population that can give rise to multiple mesenchymal phenotypes
and that facilitates hematopoietic recovery. We characterized NA-BMCs by flow cytometry, fibroblast colony-forming units (CFU-f),
real-time PCR, and in in vivo experiments. In comparison to adherent cells, NA-BMCs expressed high levels of CD11b+ and CD90+ within the CD45+ cell fraction. CFU-f were significantly declining over the cultivation period, but NA-BMCs were still able to form CFU-f
after 5 days. Gene expression analysis of allogeneic NA-BMCs compared to bone marrow (BM) indicates that NA-BMCs contain stromal,
mesenchymal, endothelial cells and monocytes, but less osteoid, lymphoid, and erythroid cells, and hematopoietic stem cells.
Histopathological data and analysis of weight showed an excellent recovery and organ repair of lethally irradiated mice after
NA-BMC transplantation with a normal composition of the BM. 相似文献
7.
Nadja Mannowetz Sabine Kartarius Gunther Wennemuth Mathias Montenarh 《Cellular and molecular life sciences : CMLS》2010,67(22):3905-3913
Protein kinase CK2 is an ubiquitously expressed enzyme that is absolutely necessary for the survival of cells. Besides the
holoenzyme consisting of the regulatory β-subunit and the catalytic α- or α′-subunit, the subunits exist in separate forms.
The subunits bind to a number of other cellular proteins. We show the expression of individual subunits as well as interaction
with the transitional nuclear protein TNP1 and with the motor neuron protein KIF5C during spermatogenesis. TNP1 is a newly
identified binding partner of the α-subunit of CK2. CK2α and KIF5C were found in late spermatogenesis, whereas CK2β and TNP1
were found in early spermatogenesis. CK2α, CK2α′, TNP1, and KIF5C were detected in the acrosome of spermatozoa, while CK2β
was detectable in the mid-piece. Combinations of CK2 subunits might determine interactions with other proteins during spermatogenesis.
KIF5C as a kinesin motor neuron protein is probably involved in the redistribution of proteins during spermatogenesis. 相似文献
8.
Lysyl oxidase is essential for hypoxia-induced metastasis 总被引:1,自引:0,他引:1
Erler JT Bennewith KL Nicolau M Dornhöfer N Kong C Le QT Chi JT Jeffrey SS Giaccia AJ 《Nature》2006,440(7088):1222-1226
Metastasis is a multistep process responsible for most cancer deaths, and it can be influenced by both the immediate microenvironment (cell-cell or cell-matrix interactions) and the extended tumour microenvironment (for example vascularization). Hypoxia (low oxygen) is clinically associated with metastasis and poor patient outcome, although the underlying processes remain unclear. Microarray studies have shown the expression of lysyl oxidase (LOX) to be elevated in hypoxic human tumour cells. Paradoxically, LOX expression is associated with both tumour suppression and tumour progression, and its role in tumorigenesis seems dependent on cellular location, cell type and transformation status. Here we show that LOX expression is regulated by hypoxia-inducible factor (HIF) and is associated with hypoxia in human breast and head and neck tumours. Patients with high LOX-expressing tumours have poor distant metastasis-free and overall survivals. Inhibition of LOX eliminates metastasis in mice with orthotopically grown breast cancer tumours. Mechanistically, secreted LOX is responsible for the invasive properties of hypoxic human cancer cells through focal adhesion kinase activity and cell to matrix adhesion. Furthermore, LOX may be required to create a niche permissive for metastatic growth. Our findings indicate that LOX is essential for hypoxia-induced metastasis and is a good therapeutic target for preventing and treating metastases. 相似文献
9.
1