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Статті в журналах з теми "HHIPL1"
Aravani, Dimitra, Elisavet Karamanavi, Sarah L. Andrews, Nilesh J. Samani, Emma J. Stringer, and Thomas R. Webb. "A The Coronary Artery Disease Associated Gene HHIPL1 Promotes Atherosclerosis." Heart 102, Suppl 6 (June 2016): A145—A146. http://dx.doi.org/10.1136/heartjnl-2016-309890.220.
Повний текст джерелаAravani, Dimitra, Gavin E. Morris, Peter D. Jones, Helena K. Tattersall, Elisavet Karamanavi, Michael A. Kaiser, Renata B. Kostogrys, et al. "HHIPL1 , a Gene at the 14q32 Coronary Artery Disease Locus, Positively Regulates Hedgehog Signaling and Promotes Atherosclerosis." Circulation 140, no. 6 (August 6, 2019): 500–513. http://dx.doi.org/10.1161/circulationaha.119.041059.
Повний текст джерелаDuong, Cuong V., Richard D. Emes, Frank Wessely, Kiren Yacqub-Usman, Richard N. Clayton, and William E. Farrell. "Quantitative, genome-wide analysis of the DNA methylome in sporadic pituitary adenomas." Endocrine-Related Cancer 19, no. 6 (October 8, 2012): 805–16. http://dx.doi.org/10.1530/erc-12-0251.
Повний текст джерелаHoltz, Alexander M., Samuel C. Griffiths, Samantha J. Davis, Benjamin Bishop, Christian Siebold, and Benjamin L. Allen. "Secreted HHIP1 interacts with heparan sulfate and regulates Hedgehog ligand localization and function." Journal of Cell Biology 209, no. 5 (June 8, 2015): 739–58. http://dx.doi.org/10.1083/jcb.201411024.
Повний текст джерелаFreixas, Xavier, and Cornelia Holthausen. "Interbank Market Integration under Asymmetric Information." Review of Financial Studies 18, no. 2 (August 18, 2004): 459–90. http://dx.doi.org/10.1093/rfs/hhi001.
Повний текст джерелаLiu, Jun, Jun Pan, and Tan Wang. "An Equilibrium Model of Rare-Event Premia and Its Implication for Option Smirks." Review of Financial Studies 18, no. 1 (November 3, 2004): 131–64. http://dx.doi.org/10.1093/rfs/hhi011.
Повний текст джерелаPost, Thierry, and Haim Levy. "Does Risk Seeking Drive Stock Prices? A Stochastic Dominance Analysis of Aggregate Investor Preferences and Beliefs." Review of Financial Studies 18, no. 3 (2005): 925–53. http://dx.doi.org/10.1093/rfs/hhi021.
Повний текст джерелаGervais, Simon, Anthony W. Lynch, and David K. Musto. "Fund Families as Delegated Monitors of Money Managers." Review of Financial Studies 18, no. 4 (2005): 1139–69. http://dx.doi.org/10.1093/rfs/hhi031.
Повний текст джерелаLiang, Guangchao, and Charles Edwin Webster. "Phosphoramidate hydrolysis catalyzed by human histidine triad nucleotide binding protein 1 (hHint1): a cluster-model DFT computational study." Org. Biomol. Chem. 15, no. 40 (2017): 8661–68. http://dx.doi.org/10.1039/c7ob02098h.
Повний текст джерелаLao, Taotao, Zhiqiang Jiang, Jeong Yun, Weiliang Qiu, Feng Guo, Chunfang Huang, John Dominic Mancini, et al. "Hhip haploinsufficiency sensitizes mice to age-related emphysema." Proceedings of the National Academy of Sciences 113, no. 32 (July 21, 2016): E4681—E4687. http://dx.doi.org/10.1073/pnas.1602342113.
Повний текст джерелаДисертації з теми "HHIPL1"
Aravani, Dimitra. "Functional analysis of the coronary artery disease associated gene HHIPL1." Thesis, University of Leicester, 2017. http://hdl.handle.net/2381/39349.
Повний текст джерелаChen, Xiangzhen Hannah. "Hedgehog-interacting protein (Hhip) as a candidate Foxn1 target in the thymus." Thesis, University of Oxford, 2017. https://ora.ox.ac.uk/objects/uuid:298cde9e-be8f-428b-9cbf-3a6b4d4e6a33.
Повний текст джерелаSizemore, Steve. "Urban eco-villages as an alternative model to revitalizing urban neighborhoods the eco-village approach of the Seminary Square/Price Hhill eco-village of Cincinnati, Ohio /." Cincinnati, Ohio : University of Cincinnati, 2004. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=ucin1085610666.
Повний текст джерела張奇華. "The expression feature of hhil gene in Hz-l virus." Thesis, 2004. http://ndltd.ncl.edu.tw/handle/13181663222994504635.
Повний текст джерелаJen, Lin Ho, and 林合真. "The functional characteristics of hhi1 gene promoter of Hz-1 virus." Thesis, 2005. http://ndltd.ncl.edu.tw/handle/46363094300679048323.
Повний текст джерела南台科技大學
生物科技系
93
The Hz-1 virus is a member of insect baculovirus, which can establish both persistent and productive infection in several lepidopteran cell lines. One results revealed that both heat and UV treatments of Hz-1 virus reduced the enhancement of hhi1 promoter activity indicating that the protein(s) on the nucleocapsid was candidate of activator to enhance the expression of hhi1. We further cloned Hz1V011 and Hz1V046, the two ORFs showing homologies to two baculovirus structure proteins: p74 and vp91-capsid associated protein, and performed cotransfection of pKS/hsp-V011 and pKS/hsp-V046 with a plasmid which expressed luciferase gene by hhi1 promoter (-688/+277) respectively. The results showed that both Hz1V011 and Hz1V046 could activate hhi1 promoter (-688/+277). Previous studies of temporal hhi1 promoter activity revealed that hhi1 promoter activity decreased from (-688/+277) to (-403/+277). These results strongly suggested that activator(s) bind to hhi1 promoter at region between –688 and -403. The computer similarity analysis of region between –688 and -403 with database of HGP in Japan showed 100% identity of five motifs: HSF (-592/-588, and –645/-641), CdxA (-480/-485), AML-1a (-655/-660, -578/-584), within –688/-403. We subjected gel mobility shift assay with fragment (–688/-557) labeled with Cy-3, however, failed to find any protein binding to this region. In order to study the profile of HHI1 during viral infection, we prepared an antibody generated by injecting New Zealand white rabbit with antigen covering amino acid number 200 to 400 of HHI1. From the results of Western blot, a 40-kd subunit was detected by 12 hours after Hz-1 viral infection and decreased 24 hours after infection. This data suggested that HHI1 protein could be cleavaged during viral infection.
Wu, Yueh-Lung, and 吳岳隆. "Regulatory and functional studies of baculovirus early genes using hhi1 and lef2." Thesis, 2008. http://ndltd.ncl.edu.tw/handle/41689171726534556004.
Повний текст джерела國立成功大學
生物科技研究所碩博士班
96
Previously we found that the upstream region of polh gene of baculovirus can induce a high level background expression of the CMVm promoter, therefore impossible to establish a tetracycline regulatory expression system (TRES) in baculovirus. In this study, we disrupted this upstream region of the polh gene, and for the first time successfully constructed a TRES in the genome of the baculovirus AcMNPV. We have used this system to regulate the expression of one of the early gene of baculovirus, lef2. LEF2 is one of the 18 late expression factors found in AcMNPV. Its cellular function is not yet fully understood, however, it is known that all lefs genes plays important roles during late and very late gene expression stages in baculovirus life cycle. We have over-expressed lef2 gene using the TRES, and discovered a ten-fold up-regulation of the polh promoter. The inducible TRES is therefore a useful tool in examining the cellular function of a particular baculovirus gene, as well as for stimulating the late or very late baculovirus promoters (p10 or polh) for protein expression. Another focus of this study is finding the early gene regulating mechanism of the HzNV-1 virus. HzNV-1 is a type viral species which can produce both latent and productive infections in insect cells. Previously, our laboratory have identified two highly-expressed transcripts, HzNV-1 Hind III-1 (hhi1) and persistency-associated gene 1 (pag1), from the HzNV-1 infected Trichoplusia ni TN-368 cells. In Sf-21 cells, the hhi1 gene can be activated by either AcMNPV or HzNV-1 virus infection. By co-transfection with AcMNPV viral DNA, we identified the active promoter region to be -62~+227 of the hhi1 gene. By progressive deletion of viral genomic DNA, we found two AcMNPV genes, ie1 and p35, together played an important role in hhi1 gene activation. Microarray study showed that two AcMNPV early genes, orf21 and orf25, also regulated by the co-operation between IE1 and P35, suggesting this co-operative gene regulation mechanism using ie1 and p35 gene products also occurred in the regulation of AcMNPV genome. We therefore discovered a new gene regulation mechanism within the AcMNPV genome. The co-operation between ie1 and p35 is not only up-regulates hhi1 gene expression, but also regulates early gene expression in the genome of AcMNPV. We also demonstrated that the expression of hhi1 gene in Sf-21 cells was sufficient to induce apoptotic cell death, mainly via the caspase 3 dependent pathway. Currently, two genes, the Hz-iap2 and PAT1 from HzNV-1, can inhibit hhi1-induced apoptosis.
Chang, Fu-Jung, and 張芙蓉. "Molecular Analysis of The Early Gene hhi1 of Insect Hz-1 Virus." Thesis, 1996. http://ndltd.ncl.edu.tw/handle/77790405325165048851.
Повний текст джерела國立臺灣師範大學
生物學系
84
Hz-1 virus is an insect virus. It can induce both productive and persistent viral infections in the Lepidopteran culture cells. In order to understand the molecular switches of productive and persistent viral infections, gene expression and regulation specifically associated to these two phases should be compared. During persistent viral infection, there is only one gene, the persistence-associated gene 1(pag1), is expressed. Since pag1 is also expressed as an immediate early (IE) gene during productive viral infection, it is necessary to compare pag1 and other productive specific IE genes to illucidate the controlling mechanisms as why all the other productive-specific IE genes are turned off during persistent viral infection but not the pag1 gene. Most of the immediate early genes of Hz-1 virus were found to locate in Hind III A, D, and I fragments previously. In this study, a sequence of 7704 base pair region has been determined in Hind III-I fragment. Computer analysis revealed the presence of two Open Reading Frames(ORF) of 1851 bp and 3426 bp onthis region. Between two ORFs, a 431 bp gap region was found. The 3''-RACE study showed the 3'' end of hhi1 gene is located at nucleotide 7478.TestCode analysis of hhi1 gene and the result of RT-PCR showed that the gap region between these two ORFs is not removed by splicing. Forthermore, in vitro translation assay also revealed that a 226 KD protein could be generated by hhi1 gene suggesting that it is resulted by a single ORF of 5670 base long.
Nchienzia, Henry. "Hedgehog interacting protein (Hhip) regulates both pancreatic and renal dysfunction in high fat diet-induced obese mouse model." Thèse, 2019. http://hdl.handle.net/1866/23524.
Повний текст джерелаHedgehog interacting protein (Hhip), a signaling molecule in the Hedgehog Hh pathway, was originally discovered as a putative antagonist of all 3 secreted Hh ligands, i.e., Sonic (Shh), Indian (Ihh), and Desert (Dhh). Hhip regulates cell function via either canonical- or non-canonical Hh pathway. Hhip encodes a protein of 700 amino acids, and is abundantly expressed in vascular endothelial cell-rich tissues, including the pancreas, and kidneys. To date, less is known about Hhip’s expression pattern in mature islet cells, and its function under normal and/or disease conditions, such as diet induced-obesity, as well as its role in chronic kidney disease, and kidney dysfunction. Hhip null mice (Hhip-/-) display markedly impaired pancreatic islet formation (45% reduction of islet mass with a decrease of beta cell proliferation by 40%), however Hhip-/- mice die shortly after birth mainly due to lung defects. In our first study, we systemically studied the role of pancreatic Hhip expression by using a whole body knock out in response to 8 weeks high fat diet (HFD) insult, and HFD-mediated beta cell dysfunction in vivo, ex vivo and in vitro using heterozygous (Hhip+/-) vs. wild type (Hhip+/+) mice. Both HFD-fed Hhip+/+ male and female mice developed severe glucose intolerance (IPGTT), which was ameliorated in male and female HFD-Hhip+/- mice. Associated with this glucose intolerance, was hyperinsulinemia, which was observed only in HFD-fed male Hhip+/- mice. HFD-fed Hhip+/- mice had high levels of circulating plasma insulin in both insulin secretion phases compared to HFD fed Hhip+/+ mice. In the pancreas, Hhip expression was increased in the islets of HFD-Hhip+/+ mice, mainly co-localized in beta cells and none in alpha cells. While maintaining the total islet number, and beta cell mass, male HFD-Hhip+/+ mice had a higher number of larger islets, in which insulin content was reduced; islet architecture was disoriented, with evident invasion of alpha cells into the central core of beta cells; and an evident increase in oxidative stress markers (8-OHdG and NADPH oxidase 2 (Nox 2)). In contrast, male HFD-Hhip+/- mice had a higher number of smaller islets, with increased beta cell proliferation, pronounced glucose stimulated insulin secretion (GSIS), ameliorated oxidative stress and preserved islet integrity. In vitro, recombinant Hhip (rHhip) dose-dependently increased oxidative stress (Nox2 and NADPH activity), and decreased the number of insulin-positive beta cells, while siRNA-Hhip enhanced GSIS, and abolished the stimulation of sodium palmitate (PA)-BSA on Nox2 gene expression. We believe our data highlights a novel finding as to how pancreatic Hhip gene inhibits insulin secretion, by altering islet integrity, and promoting Nox2 gene expression in beta cells in response to HFD-mediated beta cell dysfunction. Diabetes presents high risk factors associated with complications such as chronic kidney disease (CKD) characterized by a gradual loss in kidney function. The increased incidence of diabetic related kidney complications has been recently correlated with increase rate of obesity. We recently established that impaired nephrogenesis in kidneys of offsprings of our murine model of maternal diabetes was associated with upregulation of Hhip gene expression [127]. Subsequently, our recent data also shows that hyperglycemia induced increased renal Hhip gene expression in adult murine kidneys leading to apoptosis of glomerular epithelial cells and endothelial to mesenchymal transition (Endo-MT) - related renal fibrosis [128]. In this current study, we demonstrated how Hhip overexpression in renal proximal tubular cells, contributes to early development of chronic kidney disease after 14 weeks of HFD. Mice in HFD-fed groups showed significantly greater weight gain as compared to mice in ND fed groups. IPGTT revealed that HFD fed mice also developed glucose intolerance, with no apparent changes in insulin sensitivity. HFD did not impact hypertension, even though we had a modest trend of increase in perirenal fat deposit in the HFD fed subgroups. Renal function as measured by the glomerular filtration rate was normal in all four subgroups, indicating that neither HFD, nor Hhip overexpression promoted renal hyperfiltration. Nonetheless, renal morphology revealed HFD kidneys had subclinical injury, presented signs of tubular vacuolization and damage compared to ND fed mice. This pathology of tubular damage and vacuolization was more pronounced in HFD-fed transgenic (Hhip-Tg) mice compared to non-Tg mice, and this promoted mild tubular cell apoptosis and enhanced oxidative stress. In conclusion, HFD feeding-induced obesity led to detrimental effects on glucose toleranc,e and mild morphological changes in kidneys, characterized by the presence of osmotic nephrosis, increased renal oxidative stress, and apoptosis which might be mediated by an increase in renal FABP4. This was exacerbated by the over-expression of Hhip in the renal proximal tubules.
Zhao, Xinping. "Le rôle de la protéine interagissant avec hedgehog (Hhip) dans la formation rénale modulée par le diabète maternel et dans la néphropathie diabétique." Thèse, 2019. http://hdl.handle.net/1866/21850.
Повний текст джерелаKuo, Ting-Yu, and 郭庭育. "Hedgehog-Interacting Protein (HHIP) Is a Key Repressor of Hedgehog Signaling Pathway that Regulates Proliferation and Invasion through HGF-cMET Pathway in Lung Adenocarcinoma." Thesis, 2014. http://ndltd.ncl.edu.tw/handle/65887976717623104752.
Повний текст джерела國立陽明大學
生化暨分子生物研究所
102
The cross-talk between oncogenic pathways and stemness pathways play important roles in tumor initiation and progression. Recent years, the aberrant activations of stemness signaling such as Hedgehog (HH), hypoxia-inducible factor, and Wnt pathways, and the stemness factors like Oct-4 and Sox-2 have been reported in lung cancers. However, most researches to date focused on the impact of positive regulators of stemness pathways in oncogenesis, but less on the importance of negative regulators. Hedgehog interaction protein (HHIP) is a membrane protein that binds to HH ligands with an affinity comparable to Ptch-1 (the native HH ligand receptor), and HHIP overexpression attenuates HH signaling by capturing HH ligands. HHIP has been found to be down-regulated in several types of cancers through promoter hyper-methylation. In lung cancer, however, its role and importance has not been identified. Here, we show that HHIP was significantly repressed in lung cancer cell lines and human lung tumor samples through epigenetic silencing. Overexpression of HHIP in lung cancer cells blocked the auto-loop induction of endogenous HH pathway, and inhibited the invasiveness of cancer cells. We also found that in starvation state, HH pathway was autonomously induced which then mediated the expression of HGF and cMET phosphorylation, while HHIP overexpression blocked such inductions and significantly repressed cell proliferation rate. Furthermore, HHIP reduced the size of spheroids formed by lung cancer cells in serum-free 3D matrix. In summary, our results indicate that HHIP is a key regulator of HH signaling that was silenced in lung cancer and thus potentiates cancer cells to activate HH stemness pathway in adverse conditions to acquire survival and metastasis abilities.
Книги з теми "HHIPL1"
400, Boston. Summary of community conversations in mission hill. 1998.
Знайти повний текст джерелаЧастини книг з теми "HHIPL1"
Gao, Min, Zhen Liu, and Renhe Zhou. "Design Evaluation Method to HHIPS Based on Ergonomics Analysis." In Lecture Notes in Electrical Engineering, 719–24. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-6232-2_85.
Повний текст джерелаТези доповідей конференцій з теми "HHIPL1"
Foreman, Marilyn G., Craig P. Hersh, Carla Grabianowski, Dawn DeMeo, Gerard J. Criner, and Edwin K. Silverman. "CHRNA3/5, IREB2, And HHIP Are Associated With COPD In African Americans." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a2895.
Повний текст джерелаZHOU, XIAOBO, Michael H. Cho, Sunita Sharma, John D. Mancini, Ke Lu, Kelan Tantisira, Benjamin A. Raby, et al. "Localizing A Chronic Obstructive Pulmonary Disease Susceptibility Genetic Determinant That Regulates Hhip." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a6015.
Повний текст джерелаHardin, Megan, Jan Zielinski, Emily S. Wan, Craig P. Hersh, Eric Schwinder, Pawel Sliwinski, Iona Hawrylkiewicz, Michael H. Cho, and Edward K. Silverman. "HHIP, CHRNA3/5 And IREB2 Are Associated With Severe COPD In Poland." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a1757.
Повний текст джерелаKim, Woo Jin, Seon-Sook Han, Yeon-Mok Oh, and Sang Do Lee. "Association Of Genetic Variants In HHIP With Lung Function In COPD Subjects." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a5867.
Повний текст джерелаYun, J. H., C. Lee, T. Liu, S. Liu, W. Qiu, E. Kim, S. Xu, et al. "Lymphocytic Inflammation in COPD: Insights from HHIP Haploinsufficient Mouse Model of Age-Associated Emphysema." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a4373.
Повний текст джерелаArroyo Varela, M., E. Salcedo Lobera, G. E. González Angulo, R. Larrosa Jiménez, and R. Bautista Moreno. "Study of the expression of the IREB2, HHIP, and FAM13A genes in COPD and lung cancer." In ERS International Congress 2022 abstracts. European Respiratory Society, 2022. http://dx.doi.org/10.1183/13993003.congress-2022.2561.
Повний текст джерелаPilarsky, Christian, Tobias Gorille, Felix Rückert, Robert Grützmann, and Hans Detlev Saeger. "Abstract 5106: A HHIP derived gene expression signature for the prediction of patient survival after adjuvant chemotherapy of pancreatic cancer." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-5106.
Повний текст джерелаHanna, R. N., K. Zerrouki, X. Xiong, P. Sanders, M. Y. Yang, L. Eldridge, R. Dagher, et al. "Evaluation of the Role of Hedgehog Interacting Protein (HHIP) and the Sonic Hedgehog Pathway to Enhance Respiratory Repair and Function in Chronic Obstructive Pulmonary Disease (COPD)." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a4062.
Повний текст джерела