Добірка наукової літератури з теми "Hedgehog interacting protein"
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Статті в журналах з теми "Hedgehog interacting protein"
Vogt, Annika, Pao-Tien Chuang, Jennifer Hebert, Jimmy Hwang, Ying Lu, Levy Kopelovich, Mohammad Athar, David R. Bickers, and Ervin H. Epstein. "Immunoprevention of Basal Cell Carcinomas with Recombinant Hedgehog-interacting Protein." Journal of Experimental Medicine 199, no. 6 (March 15, 2004): 753–61. http://dx.doi.org/10.1084/jem.20031190.
Повний текст джерелаBishop, Benjamin, A. Radu Aricescu, Karl Harlos, Chris A. O'Callaghan, E. Yvonne Jones, and Christian Siebold. "Structural insights into hedgehog ligand sequestration by the human hedgehog-interacting protein HHIP." Nature Structural & Molecular Biology 16, no. 7 (June 28, 2009): 698–703. http://dx.doi.org/10.1038/nsmb.1607.
Повний текст джерелаSekiguchi, Haruki, Masaaki Ii, Kentaro Jujo, Marie-Ange Renault, Tina Thorne, Trevor Clarke, Aiko Ito, et al. "Estradiol triggers sonic-hedgehog-induced angiogenesis during peripheral nerve regeneration by downregulating hedgehog-interacting protein." Laboratory Investigation 92, no. 4 (February 13, 2012): 532–42. http://dx.doi.org/10.1038/labinvest.2012.6.
Повний текст джерелаTojo, M., H. Kiyosawa, K. Iwatsuki, and F. Kaneko. "Expression of a sonic hedgehog signal transducer, hedgehog-interacting protein, by human basal cell carcinoma." British Journal of Dermatology 146, no. 1 (January 2002): 69–73. http://dx.doi.org/10.1046/j.1365-2133.2002.04583.x.
Повний текст джерелаCobourne, Martyn, and Paul Sharpe. "Expression and Regulation of Hedgehog-Interacting Protein During Early Tooth Development." Connective Tissue Research 43, no. 2 (April 1, 2002): 143–47. http://dx.doi.org/10.1080/713713516.
Повний текст джерелаCobourne, Martyn T., and Paul T. Sharpe. "Expression and Regulation of Hedgehog-Interacting Protein During Early Tooth Development." Connective Tissue Research 43, no. 2-3 (January 2002): 143–47. http://dx.doi.org/10.1080/03008200290000907.
Повний текст джерелаVan Durme, Y. M. T. A., M. Eijgelsheim, G. F. Joos, A. Hofman, A. G. Uitterlinden, G. G. Brusselle, and B. H. C. Stricker. "Hedgehog-interacting protein is a COPD susceptibility gene: the Rotterdam Study." European Respiratory Journal 36, no. 1 (December 8, 2009): 89–95. http://dx.doi.org/10.1183/09031936.00129509.
Повний текст джерелаLu, Jiuyi, Minyong Chen, Xiu-Rong Ren, Jiangbo Wang, H. Kim Lyerly, Larry Barak, and Wei Chen. "Regulation of Hedgehog Signaling by Myc-Interacting Zinc Finger Protein 1, Miz1." PLoS ONE 8, no. 5 (May 3, 2013): e63353. http://dx.doi.org/10.1371/journal.pone.0063353.
Повний текст джерелаCoulombe, J., E. Traiffort, K. Loulier, H. Faure, and M. Ruat. "Hedgehog interacting protein in the mature brain: membrane-associated and soluble forms." Molecular and Cellular Neuroscience 25, no. 2 (February 2004): 323–33. http://dx.doi.org/10.1016/j.mcn.2003.10.024.
Повний текст джерелаKobune, M., S. Iyama, S. Kikuchi, H. Horiguchi, T. Sato, K. Murase, Y. Kawano, et al. "Stromal cells expressing hedgehog-interacting protein regulate the proliferation of myeloid neoplasms." Blood Cancer Journal 2, no. 9 (September 2012): e87-e87. http://dx.doi.org/10.1038/bcj.2012.36.
Повний текст джерелаДисертації з теми "Hedgehog interacting protein"
Chen, 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 джерелаTruong, Sarah. "Non-canonical activation of Hedgehog signaling in prostate cancer cells is mediated by the interaction of Gli proteins and transcriptionally active androgen receptor." University of British Columbia, 2017. http://hdl.handle.net/2429/64120.
Повний текст джерелаMedicine, Faculty of
Graduate
Bruzzone, Lucía. "A crosstalk between the RNA binding protein Smaug and the Hedgehog pathway links cell signaling to mRNA regulation in drosophila." Thesis, Sorbonne Paris Cité, 2018. https://theses.md.univ-paris-diderot.fr/BRUZZONE_Lucia_1_va_20180319.pdf.
Повний текст джерелаPost-transcriptional regulation of gene expression plays a critical role in a variety of cellular processes during development. RNA binding proteins are fundamental mediators of post-transcriptional regulations that control mRNA expression by recognizing specific cis acting elements within the target transcripts. Smaug is a highly conserved sequence specific RNA-binding protein that is essential during Drosophila early embryogenesis. Smaug binds Smaug Recognition Elements (SRE) in the target mRNA and recruits additional factors, via protein-protein interactions, that regulate the bound mRNA. An emergent concept that signaling pathways can modulate RBP activity by post-translation modifications adds a new layer in the control of gene expression. During my thesis work, I sought to understand how the Hedgehog pathway regulates Smaug by promoting its phosphorylation. My work shows that HH signaling downregulates Smaug protein levels affecting its ability to repress mRNA translation. This negative effect seems to be dependent on the interaction between Smaug and the HH signal transducer Smoothened. Moreover, Smaug is constitutively phosphorylated in its RNA binding domain, which appears to be necessary for cytoplasmic Smaug foci formation
Kuo, 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.
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.
Книги з теми "Hedgehog interacting protein"
Hedgehog signaling activation in human cancer and its clinical implications. New York: Springer, 2011.
Знайти повний текст джерелаXie, Jingwu. Hedgehog signaling activation in human cancer and its clinical implications. Springer, 2014.
Знайти повний текст джерелаЧастини книг з теми "Hedgehog interacting protein"
Tong, Chao, and Jin Jiang. "Using Immunoprecipitation to Study Protein–Protein Interactions in the Hedgehog-Signaling Pathway." In Methods in Molecular Biology, 215–29. Totowa, NJ: Humana Press, 2007. http://dx.doi.org/10.1007/978-1-59745-516-9_15.
Повний текст джерелаFu, Lin, Xiangdong Lv, Yue Xiong, and Yun Zhao. "Investigation of Protein–Protein Interactions and Conformational Changes in Hedgehog Signaling Pathway by FRET." In Methods in Molecular Biology, 61–70. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2772-2_6.
Повний текст джерелаТези доповідей конференцій з теми "Hedgehog interacting protein"
Yun, J. H., S. Han, J. Platig, A. X. Zhou, and J. Lu. "Differentially Correlated Molecular Pathways with Hedgehog Interacting Protein in Human and Mouse Lungs." In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a4658.
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 джерелаBian, Liming, Robert L. Mauck, and Jason A. Burdick. "Dynamic Compressive Loading and Crosslinking Density Influence the Chondrogenic and Hypertrophic Differentiation of Human Mesenchymal Stem Cells Seeded in Hyaluronic Acid Hydrogels." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80048.
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