共查询到20条相似文献,搜索用时 156 毫秒
1.
2.
Loss-of function mutations in the transmembrane inner ear expressed (Tmie/TMIE) gene have been shown to cause deafness in mice and humans (DFNB6). Previous studies report that the circling mouse can be an animal model for DFNB6. However, the expression pattern of Tmie protein in postnatal developmental stages has not been clearly revealed. In this study we tried to investigate the expression of Tmie protein in the liver, spleen, kidney, and lung, as well as in the cochlea. We examined various tissue samples from five different age groups of C57BL/6J animals. Using western blotting analysis, the expression of Tmie protein in these organs has been identified. The results show that Tmie protein expression in the cochlea has been increased in postnatal developmental stages, indicating that Tmie plays an important role in not only the development and also in the function of the cochlea. The expression pattern of Tmie in adult mouse organs such as the liver, spleen, kidney, and spleen significantly vary in adult rats. The order of Tmie expression level in mice (63 days after birth) was spleen, liver, lung, cochlea, and kidney, whereas in the adult rat it was liver, cochlea, lung, spleen, and kidney. 相似文献
3.
Wei Li Zu-Xi Yu Robert M Kotin 《The journal of histochemistry and cytochemistry》2005,53(8):1003-1009
Protein kinase X (PrKX), karyotypically located on the human X chromosome, is a type I cAMP-dependent protein kinase. Although a specific role for PrKX has not yet been defined, PrKX gene expression in mouse and human tissues has been profiled only by in situ hybridization and Northern blot analyses and not by protein expression. To determine more precisely the PrKX protein levels, we developed specific anti-PrKX antibodies and examined gestationally staged mouse embryo sections by immunohistochemistry. These results showed that PrKX is ubiquitously distributed and highly expressed in murine central nervous system and heart tissues in early developmental stages and in most organs at later stages but was not detected in either connective tissues or bone. Using Western blots to detect PrKX, total protein extracts from eight different adult or fetal human tissues including brain, heart, kidney, liver, lung, pancreas, spleen, and thymus were analyzed. Although PrKX protein was present in each of the tissues tested, the protein levels varied depending on tissue type and developmental stage. Very low protein levels were found in heart tissues from a 5-month-old fetus and from an adult, whereas PrKX proteins were more abundant in fetal brain, kidney, and liver tissues compared with adult samples of the same tissue type. 相似文献
4.
肝细胞生长因子mRNA在成年小鼠和人胎儿不同器官中的表达 总被引:2,自引:0,他引:2
本实验从成年小鼠和胎龄4-5月的人胎儿不同器官中分离总RNA。经斑点印迹分析显示,肝细胞生长因子(HGF)mRNA在成年KM小鼠多种器官中表达,其表达水平由高到低依次为:肺、肝、肾、卵巢、睾丸、大脑和胃;在脾、心、骨髓、小肠和骨骼肌组织中以HGFmRNA。在胎龄4-5月的人胎儿中,HGFmRNA表达水平由高到低依次为:大脑、肝、腮腺、胃、小肠、肾、心和骨骼肌;肺和脾组织为阴性。由此可见,HGF在成 相似文献
5.
Induction of Src-suppressed C kinase substrate (SSeCKS) in vascular endothelial cells by bacterial lipopolysaccharide. 总被引:4,自引:0,他引:4
Hiroshi Kitamura Keisuke Okita Daisuke Fujikura Koshi Mori Toshihiko Iwanaga Masayuki Saito 《The journal of histochemistry and cytochemistry》2002,50(2):245-255
We isolated cDNA of the mouse homologue of the src-suppressed C kinase substrate (SSeCKS) and analyzed the effects of lipopolysaccharide (LPS) injection on the tissue expression pattern of this protein. Northern blotting analysis showed that SSeCKS mRNA was expressed abundantly in the testis but at undetectable levels in other tissues of untreated control mice. Intraperitoneal administration of LPS strongly induced SSeCKS mRNA expression in the lung, heart, liver, spleen, kidney, lymph node, adrenal gland, and pituitary gland, as well as in the brain. In lung and spleen, the SSeCKS mRNA levels increased almost 10-fold at 1 hr after LPS injection and persisted at high levels until 4 hr. Both in situ hybridization and immunohistochemical studies revealed that LPS administration conspicuously elevated expression of SSeCKS mRNA and protein in vascular endothelial cells of several organs. Ectopic expression of SSeCKS caused loss of cytoplasmic F-actin fibers in the mouse endothelial cell line LEII. These results indicate that SSeCKS is one of the major LPS-responsive proteins and may participate in alteration of cytoskeletal architecture in endothelial cells during inflammation. 相似文献
6.
7.
8.
9.
Yong-Zhen Huang Zi-Jing Zhang Hua He Xiu-Kai Cao Cheng-Chuang Song Kun-Peng Liu 《Animal biotechnology》2017,28(2):104-111
DNA methylation is essential for the regulation of gene expression and important roles in muscle development. To assess the extent of epigenetic modifications and gene expression on the differentially methylated region (DMR) in ZBED6, we simultaneously examined DNA methylation and expression in six tissues from two different developmental stages (fetal bovine and adult bovine). The DNA methylation pattern was compared using bisulfite sequencing polymerase chain reaction (BSP) and combined bisulfite restriction analysis (COBRA). The result of quantitative real-time PCR (qPCR) analysis showed that ZBED6 has a broad tissue distribution and is highly expressed in adult bovine (P?0.05 or P?0.01). The DNA methylation level was significantly different in liver, lung and spleen between the two cattle groups (P?0.05 or P?0.01). The adult bovine group exhibited a significantly higher mRNA level and lower DNA methylation level than the fetal bovine group in liver, lung, and spleen. No significant association was detected between DNA methylation level and muscle, heart, and kidney at two different stages. In this study, the statistical analyses indicated that DNA methylation patterns are associated with mRNA level in some tissues, these results may be a useful parameter to investigate muscle developmental in cattle and as a model for studies in other species, potentially contributing to an improvement of growth performance selection in beef cattle breeding program. 相似文献
10.
The isozyme pattern and total activity of adenylate kinase were studied in normal adult and fetal human and rat tissues using starch gel electrophoresis. Three adenylate kinase isoenzymes were identified in human tissues. Although normal adult lung exhibited higher adenylate kinase activity than did its fetal or neoplastic variant, isozyme patterns in the three types of tissues were indistinguishable from each other and from that in fetal human liver. The pattern of these three isozymes in rat lung (as in spleen) also did not change between fetal and adult life. However, adult kidney and heart of this species did appear to contain isozymes not present in fetal life. Brain (both adult and fetal) was striking different from all the other tissues in that it contained only one adenylate kinase isozyme. The total adenylate kinase activity per gram of adult rat liver, kidney and lung was significantly higher than in the cognate fetal organs, whereas that in brain or spleen did not change with age. The activity in adult heart (similar to the fetal one) was higher than in any other tissue examined. 相似文献
11.
12.
Expression of the Von Hippel-Lindau tumor suppressor gene,VHL, in human fetal kidney and during mouse embryogenesis.
下载免费PDF全文
![点击此处可从《Molecular medicine (Cambridge, Mass.)》网站下载免费的PDF全文](/ch/ext_images/free.gif)
P. M. Kessler S. P. Vasavada R. R. Rackley T. Stackhouse F. M. Duh F. Latif M. I. Lerman B. Zbar B. R. Williams 《Molecular medicine (Cambridge, Mass.)》1995,1(4):457-466
BACKGROUND: Von Hippel-Lindau (VHL) disease is a familial cancer syndrome that has a dominant inherited pattern which predisposes affected individuals to a variety of tumours. The most frequent tumors are hemangioblastomas of the central nervous system and retina, renal cell carcinoma (RCC), and pheochromocytoma. The recent identification and characterization of the VHL gene on human chromosome 3p and mutational analyses confirms the VHL gene functions as a classical tumor suppressor. Not only are mutations in this gene responsible for the VHL syndrome, but mutations are also very frequent in sporadic RCC. MATERIALS AND METHODS: VHL expression in human kidney and during embryogenesis, was analyzed by in situ mRNA hybridization with 35S-labeled antisense VHL probes, derived from human and mouse cDNAs, on cryosections of human fetal kidney and paraffin sections of murine embryos. RESULTS: In human fetal kidney, there was enhanced expression of VHL within the epithelial lining of the proximal tubules. During embryogenesis, VHL expression was ubiquitous in all three germ cell layers and their derivatives. Expression occurred in the cerebral cortex, midbrain, cerebellum, retina, spinal cord, and postganglionic cell bodies. All organs of the thoracic and abdominal cavities expressed VHL, but enhanced expression was most apparent in the epithelial components of the lung, kidney, and eye. CONCLUSIONS: In human fetal kidney, the enhanced epithelial expression of the VHL gene is consistent with the role of this gene in RCC. There is widespread expression of the VHL gene during embryogenesis, but this is pronounced in areas associated with VHL phenotypes. These findings provide a histological framework for investigating the physiological role of the VHL gene and as basis for further mutational analysis. 相似文献
13.
14.
Ulrike Teichmann Michael E. Ray Jane Ellison Caroline Graham Graeme Wistow Paul S. Meltzer Jeffrey M. Trent William J. Pavan 《Mammalian genome》1998,9(9):715-720
We report the isolation of the murine ortholog of AIM1, a human gene whose expression is associated with the reversal of
tumorigenicity in an experimental model of melanoma. Mouse and human AIM1 are more than 90% identical in amino acid sequence
in the βγ-crystallin repeats and the C-terminal domain, and more than 75% identical in the extended N-terminal domain. Consistent
with the isolated cDNA representing the authentic AIM1 ortholog, linkage analysis localized mouse Aim1 to proximal mouse Chromosome (Chr) 10 in a conserved linkage group with genes localized to human Chr band 6q21. Searches
of EST databases identified a second AIM1-like gene in both mouse and human, suggesting the existence of a gene family. Northern
analysis demonstrates Aim1 is expressed most abundantly in adult skin, lung, heart, liver, and kidney and is temporally regulated during embryogenesis.
Aim1 is expressed highly in the shaft region of the hair follicles and the presumptive ectoderm, but not at detectable levels
in melanocytes or melanocyte precursor cells.
Received: 18 February 1998 / Accepted: 8 May 1998 相似文献
15.
16.
17.
18.
H Werner M Adamo W L Lowe C T Roberts D LeRoith 《Molecular endocrinology (Baltimore, Md.)》1989,3(2):273-279
The developmental regulation of rat brain-derived/Hep G2 glucose transporter gene expression was studied by means of Northern blot hybridization, using a rat brain glucose transporter cDNA probe, in order to directly quantify steady state glucose transporter mRNA levels. The results obtained showed different tissue-specific patterns of glucose transporter mRNA levels during ontogenesis; while in brain there was a sustained increase in the levels of the message from 20 days embryogenesis until 50 days postnatal, other organs such as heart, lung, liver, and muscle expressed maximal levels of the glucose transporter mRNA in 20-day fetuses and 1-day neonates, decreasing subsequently to very low levels. The relative expression of the glucose transporter mRNA in the different tissues, at both fetal and adult stages, was analyzed using a solution hybridization-RNase protection assay. This approach revealed that, while the heart expresses the highest levels of glucose transporter mRNA at 20 days of fetal life, the brain shows the highest levels at the adult stage. These results indicate a tissue-specific ontogenic pattern of glucose transporter gene expression, suggesting a developmental role for this glucose transporter gene product. 相似文献
19.
Irmgard S. Thorey Juanito J. Meneses Nicolay Neznanov David A. Kulesh Roger A. Pedersen Robert G. Oshima 《Developmental biology》1993,160(2)
During embryogenesis, EndoB, the mouse form of human keratin 18 (K18), is expressed in a complex spatial and temporal pattern in various embryonic epithelia. We have compared the expression of transgenic human K18 to the endogenous mouse homolog and to the coexpressed, complementary keratin 8 homolog, EndoA, during postimplantation mouse embryogenesis and fetal development in order to determine the developmental expression pattern of the human gene in a mouse environment. The tissue distribution of K18 protein was identical to that of endogenous EndoB in both 7.5- and 13.5-day-old embryos, except for certain heart, eye, and extraembryonic mesodermal tissues in which K18 was not detected. These results indicate that the 10-kb K18 gene specifies appropriate developmental expression in the mouse and support previously reported differences in K18 expression in human and mouse fetal heart. We have also compared the expression patterns of K18 to a series of constructions that utilize the Escherichia coli gene for β-galactosidase (lacZ) as a reporter gene. Some of these constructions were regulated correctly in embryos during development of the germ layers. However, none was expressed consistently in extraembryonic or in adult tissues. Analysis with methylation-sensitive restriction enzymes revealed that hypermethylation of the CpG-rich prokaryotic reporter gene was not the cause of its silence in adult transgenic liver. However, the repressed state of K18-LacZ transgenes in adult liver was correlated with a different chromatin state that lacked diagnostic DNase hypersensitive sites found in K18 transgenic liver. Expression of the lacZ reporter gene did not accurately reflect the developmental pattern of K18 even in constructions that used all available K18 sequences. We conclude that in these contexts, the lacZ gene was not a developmentally neutral reporter gene. 相似文献