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21.
Suzanne Demczuk Annie Lévy Muriel Aubry Marie-Françoise Croquette Nicole Philip Marguerite Prieur Ursula Sauer Patrice Bouvagnet Guy A. Rouleau Gilles Thomas Alain Aurias 《Human genetics》1995,96(1):9-13
We have determined the parental origin of the deleted chromosome 22 in 29 cases of DiGeorge syndrome (DGS) using a CA-repeat mapping within the commonly deleted region, and in one other case by using a chromosome 22 short arm heteromorphism. The CA-repeat was informative in 21 out of 29 families studied and the deleted chromosome was of maternal origin in 16 cases (72%). When these data are pooled with recent results from the literature, 24 de novo DGS, velo-cardio-facial syndrome (VCFS) and isolated conotruncal cardiac disease deletions are found to be of maternal origin and 8 of paternal origin, yielding a 2 of 8 with a probability level lower than 0.01. These data, and review of the literature on familial DGS/VCFS and isolated conotruncal cardiopathies suggest that there is a strong tendency for the 22q11.2 deletions to be of maternal origin. 相似文献
22.
James E. Womack Muriel T. Davisson Eva M. Eicher Debra A. Kendall 《Biochemical genetics》1977,15(3-4):347-355
A method for detecting two alleles at Np-1 (nucleoside phosphorylase) and three alleles at Es-10 (esterase 10) from mouse blood by cellulose acetate electrophoresis is described. The allelic constitution at these loci for 44 inbred strains and stocks was determined. The location of Np-1 on chromosome 14 was established by backcross experiments in which alleles at Np-1 and Robertsonian translocations were segregating. Es-10 was shown to be linked to Np-1, and the following genetic map of Chr 14 was constructed: centromere-(8.9±4.0 cM)-[Np-1, Wc]-(10.2±1.9 cM)-Es-10-(15.5±3.7 cM)-s. The homologous human loci, NP and ES-D, are not linked.This work was supported by Contract E(11-1)-3267 with the Energy Research and Development Administration, by Contracts NO1-ES4-2156 and NO1-ES4-2159 with the National Institute of Environmental Health Sciences, and by Grants GM 19656 and GM 20919 from the National Institute of General Medical Sciences. D. A. K. was a participant in the 1975 Summer Program for College, Graduate, and Medical Students, which was supported, in part, by the Clark Foundation. The Jackson Laboratory is fully accredited by the American Association for Accreditation of Laboratory Animal Care. 相似文献
23.
Peleg Leah Nesbitt Muriel N. Ashkenazi Israel E. 《Journal of comparative physiology. A, Neuroethology, sensory, neural, and behavioral physiology》1982,147(1):137-142
Journal of Comparative Physiology A - A/J mice differ from C57BL/6J mice in the time of the daily peak of activity of glyceraldehyde-3-phosphate dehydrogenase (GAPD) in thymus and in thyroid.... 相似文献
24.
25.
Prevention of kidney ischemia/reperfusion-induced functional injury, MAPK and MAPK kinase activation, and inflammation by remote transient ureteral obstruction. 总被引:11,自引:0,他引:11
Kwon Moo Park Cornelis Kramers Muriel Vayssier-Taussat Ang Chen Joseph V Bonventre 《The Journal of biological chemistry》2002,277(3):2040-2049
Protection against ischemic kidney injury is afforded by 24 h of ureteral obstruction (UO) applied 6 or 8 days prior to the ischemia. Uremia or humoral factors are not responsible for the protection, since unilateral UO confers protection on that kidney but not the contralateral kidney. Prior UO results in reduced postischemic outer medullary congestion and leukocyte infiltration. Prior UO results in reduced postischemic phosphorylation of c-Jun N-terminal stress-activated protein kinase 1/2 (JNK1/2), p38, mitogen-activated protein kinase (MAPK) kinase 4 (MKK4), and MKK3/6. Very few cells stain positively for proliferating cell nuclear antigen after obstruction, indicating that subsequent protection against ischemia is not related to proliferation with increased numbers of newly formed daughter cells more resistant to injury. UO increases the expression of heat shock protein (HSP)-25 and HSP-72. The increased HSP-25 expression persists for 6 or 8 days, whereas HSP-72 does not. HSP-25 expression is increased in the proximal tubule cells in the outer stripe of the outer medulla postobstruction, prior to, and 24 h after ischemia. In LLC-PK(1) renal epithelial cells, adenovirus-expressed human HSP-27 confers resistance to chemical anoxia and oxidative stress. Increased HSP-27 expression in LLC-PK(1) cells results in reduced H(2)O(2)-induced phosphorylation of JNK1/2 and p38. In conclusion, prior transient UO renders the kidney resistant to ischemia. This resistance to functional consequences of ischemia is associated with reduced postischemic activation of JNK, p38 MAP kinases, and their upstream MAPK kinases. The persistent increase in HSP-25 that occurs as a result of UO may contribute to the reduction in phosphorylation of MAPKs that have been implicated in adhesion molecule up-regulation and cell death. 相似文献
26.
Carlier L Couprie J le Maire A Guilhaudis L Milazzo-Segalas I Courçon M Moutiez M Gondry M Davoust D Gilquin B Zinn-Justin S 《Protein science : a publication of the Protein Society》2007,16(12):2750-2755
Human KIN17 is a 45-kDa eukaryotic DNA- and RNA-binding protein that plays an important role in nuclear metabolism and in particular in the general response to genotoxics. Its amino acids sequence contains a zinc finger motif (residues 28-50) within a 30-kDa N-terminal region conserved from yeast to human, and a 15-kDa C-terminal tandem of SH3-like subdomains (residues 268-393) only found in higher eukaryotes. Here we report the solution structure of the region 51-160 of human KIN17. We show that this fragment folds into a three-alpha-helix bundle packed against a three-stranded beta-sheet. It belongs to the winged helix (WH) family. Structural comparison with analogous WH domains reveals that KIN17 WH module presents an additional and highly conserved 3(10)-helix. Moreover, KIN17 WH helix H3 is not positively charged as in classical DNA-binding WH domains. Thus, human KIN17 region 51-160 might rather be involved in protein-protein interaction through its conserved surface centered on the 3(10)-helix. 相似文献
27.
Paget C Ivanov S Fontaine J Renneson J Blanc F Pichavant M Dumoutier L Ryffel B Renauld JC Gosset P Gosset P Si-Tahar M Faveeuw C Trottein F 《The Journal of biological chemistry》2012,287(12):8816-8829
Invariant natural killer T (iNKT) cells are non-conventional lipid-reactive αβ T lymphocytes that play a key role in host responses during viral infections, in particular through the swift production of cytokines. Their beneficial role during experimental influenza A virus (IAV) infection has recently been proposed, although the mechanisms involved remain elusive. Here we show that during in vivo IAV infection, mouse pulmonary iNKT cells produce IFN-γ and IL-22, a Th17-related cytokine critical in mucosal immunity. Although permissive to viral replication, IL-22 production by iNKT cells is not due to IAV infection per se of these cells but is indirectly mediated by IAV-infected dendritic cells (DCs). We show that activation of the viral RNA sensors TLR7 and RIG-I in DCs is important for triggering IL-22 secretion by iNKT cells, whereas the NOD-like receptors NOD2 and NLRP3 are dispensable. Invariant NKT cells respond to IL-1β and IL-23 provided by infected DCs independently of the CD1d molecule to release IL-22. In vitro, IL-22 protects IAV-infected airway epithelial cells against mortality but has no role on viral replication. Finally, during early IAV infection, IL-22 plays a positive role in the control of lung epithelial damages. Overall, IAV infection of DCs activates iNKT cells, providing a rapid source of IL-22 that might be beneficial to preserve the lung epithelium integrity. 相似文献
28.
J F Riou M Umbhauer D L Shi J C Boucaut 《Biology of the cell / under the auspices of the European Cell Biology Organization》1992,75(1):1-9
Tenascin is a large oligomeric extracellular matrix (ECM) glycoprotein whose expression is highly restricted during vertebrate development. It has a characteristic hexameric quaternary structure with six arms linked to a central globular domain. Each arm contains a single polypeptide with the central globular domain formed by the covalent association of the N-terminal ends of the six polypeptides. Tenascin first appears during development, associated with the neural crest cell migration pathways of mammalian, avian and amphibian embryos. During later development, it is observed at sites of cartilage, bone and tendon formation. Tenascin expression also occurs in defined areas in the developing nervous system and in condensing mesenchyme, in response to epithelio-mesenchymal interactions. The function of tenascin in these different morphogenetic processes is not yet clearly understood. Tenascin can promote neurite outgrowth in vitro and can inhibit cell interactions with fibronectin. Results based on antibody mapping and molecular cloning indicate that these properties involve two distinct cell binding sites. Together with its highly regulated expression in the embryo, these properties suggest that tenascin plays a key role in the control of cell migration and differentiation during development. 相似文献
29.
Kpatènon Mariano Joly Salako Kolawolé Valère Santoni Sylvain Zekraoui Leila Latreille Muriel Tollon-Cordet Christine Mariac Cédric Jaligot Estelle Beulé Thierry Adéoti Kifouli 《BMC genetics》2020,21(1):1-12
Biological pathways play an important role in the occurrence, development and recovery of complex diseases, such as cancers, which are multifactorial complex diseases that are generally caused by mutation of multiple genes or dysregulation of pathways. We propose a path-specific effect statistic (PSE) to detect the differential specific paths under two conditions (e.g. case VS. control groups, exposure Vs. nonexposure groups). In observational studies, the path-specific effect can be obtained by separately calculating the average causal effect of each directed edge through adjusting for the parent nodes of nodes in the specific path and multiplying them under each condition. Theoretical proofs and a series of simulations are conducted to validate the path-specific effect statistic. Applications are also performed to evaluate its practical performances. A series of simulation studies show that the Type I error rates of PSE with Permutation tests are more stable at the nominal level 0.05 and can accurately detect the differential specific paths when comparing with other methods. Specifically, the power reveals an increasing trends with the enlargement of path-specific effects and its effect differences under two conditions. Besides, the power of PSE is robust to the variation of parent or child node of the nodes on specific paths. Application to real data of Glioblastoma Multiforme (GBM), we successfully identified 14 positive specific pathways in mTOR pathway contributing to survival time of patients with GBM. All codes for automatic searching specific paths linking two continuous variables and adjusting set as well as PSE statistic can be found in supplementary materials. The proposed PSE statistic can accurately detect the differential specific pathways contributing to complex disease and thus potentially provides new insights and ways to unlock the black box of disease mechanisms. 相似文献
30.
Muriel Cario Catherine Pain Priscilla Kaulanjan‐Checkmodine Daniela Masia Gabriele Delia Vincent Casoli Pierre Costet Jean‐Franois Goussot Vronique Guyonnet‐Duperat Alice Bibeyran Khaled Ezzedine Corinne Reymermier Valrie Andre‐Frei Alain Taieb 《Pigment cell & melanoma research》2020,33(3):435-445
Human skin melanin pigmentation is regulated by systemic and local factors. According to the type of melanin produced by melanocytes, the transfer and degradation of melanosomes differ, thus accounting for most variations between ethnicities. We made the surprising observation that in a drastically changed environment, white and black phenotypes are reversible since Caucasian skin grafted onto nude mice can become black with all black phenotypic characteristics. Black xenografts differed essentially from other grafts by the levels of epidermal FGF‐2 and keratin 5. In vitro analysis confirmed that FGF‐2 directly regulates keratin 5. Interestingly, this phenomenon may be involved in human pathology. Keratin 5 mutations in Dowling–Degos Disease (DDD) have already been associated with the pheomelanosome–eumelanosome transition. In a DDD patient, keratin 5 was expressed in the basal and spinous layers, as observed in black xenografts. Furthermore, in a common age‐related hyperpigmentation disorder like senile lentigo (SL), keratin 5 distribution is also altered. In conclusion, modulation of keratin 5 expression and distribution either due to mutations or factors may account for the development of pigmentary disorders. 相似文献