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Статті в журналах з теми "PLEKHO1"
He, Xiaojuan, Jin Liu, Chao Liang, Shaikh Atik Badshah, Kang Zheng, Lei Dang, Baosheng Guo, et al. "Osteoblastic PLEKHO1 contributes to joint inflammation in rheumatoid arthritis." EBioMedicine 41 (March 2019): 538–55. http://dx.doi.org/10.1016/j.ebiom.2019.02.009.
Повний текст джерелаLiu, Jin, Chao Liang, Baosheng Guo, Xiaohao Wu, Defang Li, Zongkang Zhang, Kang Zheng, et al. "Increased PLEKHO1 within osteoblasts suppresses Smad-dependent BMP signaling to inhibit bone formation during aging." Aging Cell 16, no. 2 (January 13, 2017): 360–76. http://dx.doi.org/10.1111/acel.12566.
Повний текст джерелаHe, Xiaojuan, Jin Liu, Chao Liang, Shaikh Atik Badshah, Kang Zheng, Lei Dang, Baosheng Guo, et al. "Corrigendum to ‘Osteoblastic PLEKHO1 contributes to joint inflammation in rheumatoid arthritis’ [EBioMedicine 41 (2019) 538–555]." EBioMedicine 52 (February 2020): 102669. http://dx.doi.org/10.1016/j.ebiom.2020.102669.
Повний текст джерелаMa, Hong-wei, Min Xie, Ming Sun, Tian-yu Chen, Rong-rong Jin, Tian-shi Ma, Qin-nan Chen, et al. "The pseudogene derived long noncoding RNA DUXAP8 promotes gastric cancer cell proliferation and migration via epigenetically silencing PLEKHO1 expression." Oncotarget 8, no. 32 (August 5, 2016): 52211–24. http://dx.doi.org/10.18632/oncotarget.11075.
Повний текст джерелаC. Han, Eric, Yu-Chuen Huang, Jane-Ming Lin, Hui-Ju Lin, Jer-Yuarn Wu, Cheng-Chun Lee, and Fuu-Jen Tsai. "Association of the PLEKHO2 and PLEKHH1 gene polymorphisms with type 2 diabetic retinopathy in a Taiwanese population." ScienceAsia 38, no. 4 (2012): 340. http://dx.doi.org/10.2306/scienceasia1513-1874.2012.38.340.
Повний текст джерелаXing, Xiangling, Ninni Mu, Xiaotian Yuan, Na Wang, C. Christofer Juhlin, Klas Strååt, Catharina Larsson, and Dawei Xu. "PLEKHS1 Over-Expression is Associated with Metastases and Poor Outcomes in Papillary Thyroid Carcinoma." Cancers 12, no. 8 (July 31, 2020): 2133. http://dx.doi.org/10.3390/cancers12082133.
Повний текст джерелаMarwaha, Rituraj, Subhash B. Arya, Divya Jagga, Harmeet Kaur, Amit Tuli, and Mahak Sharma. "The Rab7 effector PLEKHM1 binds Arl8b to promote cargo traffic to lysosomes." Journal of Cell Biology 216, no. 4 (March 21, 2017): 1051–70. http://dx.doi.org/10.1083/jcb.201607085.
Повний текст джерелаGill, Emily, Gurimaan Sandhu, Douglas G. Ward, Claire M. Perks, and Richard T. Bryan. "The Sirenic Links between Diabetes, Obesity, and Bladder Cancer." International Journal of Molecular Sciences 22, no. 20 (October 15, 2021): 11150. http://dx.doi.org/10.3390/ijms222011150.
Повний текст джерелаTabata, Keisuke, Kohichi Matsunaga, Ayuko Sakane, Takuya Sasaki, Takeshi Noda, and Tamotsu Yoshimori. "Rubicon and PLEKHM1 Negatively Regulate the Endocytic/Autophagic Pathway via a Novel Rab7-binding Domain." Molecular Biology of the Cell 21, no. 23 (December 2010): 4162–72. http://dx.doi.org/10.1091/mbc.e10-06-0495.
Повний текст джерелаNishikawa, Masashi, Hidenori Ito, Hidenori Tabata, Hiroshi Ueda, and Koh-ichi Nagata. "Impaired Function of PLEKHG2, a Rho-Guanine Nucleotide-Exchange Factor, Disrupts Corticogenesis in Neurodevelopmental Phenotypes." Cells 11, no. 4 (February 16, 2022): 696. http://dx.doi.org/10.3390/cells11040696.
Повний текст джерелаДисертації з теми "PLEKHO1"
Dang, Lei. "Osteoblastic PLEKHO1 contributes to joint inflammation in rheumatoid arthritis." HKBU Institutional Repository, 2019. https://repository.hkbu.edu.hk/etd_oa/687.
Повний текст джерелаRunne, Caitlin M. "Function and Activation Mechanism of PLEKHG2, A Novel G Beta Gamma-Activated RhoGEF in Leukemia Cells." Diss., University of Iowa, 2013. https://ir.uiowa.edu/etd/4907.
Повний текст джерелаLeveziel, Nicolas. "Génétique de la dégénérescence maculaire liée à l'âge variants majeurs de prédisposition à la forme exsudative." Paris 6, 2008. http://www.theses.fr/2008PA066183.
Повний текст джерелаSadras, Francisco. "A role for bivalent genes in epithelial to mesenchymal transition." Thesis, 2017. http://hdl.handle.net/2440/109800.
Повний текст джерелаThesis (Ph.D.) -- University of Adelaide, School of Biological Sciences, 2017.
Chen, Ke-Wei, and 陳克偉. "Roles of PLEKHF1 in endocytosis-related processes." Thesis, 2006. http://ndltd.ncl.edu.tw/handle/93348812817055276224.
Повний текст джерела國立陽明大學
微生物及免疫學研究所
94
Based on a series of genomics analysis that targets differentially expressed genes in liver cancers, we have identified, from their distinctive endosomal localization patterns, two novel genes named PLEKHF1 (pleckstrin homology domain containing, family F (with FYVE domain) member 1, or PF1) and PLEKHF2 (PF2). Overexpression of either PF1 or PF2 resulted in the enlargement of the endosome. This study focuses on deciphering the signalling pathway underlying this intriguing phenotype of PF1. PF1 and PF2 represent two members of a new protein family called Phafins (protein containing both PH and FYVE domains), which consists of 14 genes from different species. GFP-tagged PF1 proteins were found in early endosomes and lysosomes, where they colocalized with EEA1 and LysoTracker Red, respectively, and this early endosomal localization is dependent on its FYVE domain. Increased expression of PF1 caused an enlargement of early endosome, as had been observed in cells expressing the constitutively active form of Rab5 gene. Endosomal enlargement caused by PF1 overespression was abolished by the simultaneous presence of the dominant negative Rab5, indicating that PF1 could regulate the endocytosis process in a Rab5-dependent manner. In addition, the presence of PF1 in the lysosome was reduced in cells containing the dominant negative Rab7. Transferrin uptake assay further showed that PF1 is involved in the early stages of endocytosis, but its overexpression had no effect on internalization rate. Furthermore, the C terminal sequence may comprise elements necessary for PF1 to enter lysosomal compartments. While confering PF2 the ability to enter lysosomes, the tail domain of PF1, when expressed alone, showed only minor colocalization with LysoTracker, suggesting tail domain may act in concert with upstream sequences to mediate lysosomal loclization. Taken together, our results suggested that PF1 represents a new player in Rab-mediated endocytosis precesses, as its effects on the formation of early endosomes was mediated by Rab5 signalling, whereas its continuous presence and metabolisms in the lysosome was modulated by the Rab7 signalling.We propose that PF1 may act as an adaptor functioning along the endocytic pathway through protein-lipid and possibly protein-protein interactions.
Wang, Chi-Tang, and 王啓唐. "Investigating the role of pleckstrin homology domain containing, family A member 1 (PLEKHA1) in Age-related macular degeneration(AMD)." Thesis, 2015. http://ndltd.ncl.edu.tw/handle/68389305876457615594.
Повний текст джерела國立陽明大學
生命科學系暨基因體科學研究所
103
Age-related macular degeneration (AMD) is a multifactorial disease for visual impairment in the senior population in developed countries. Clinical manifestations of AMD include the extracellular deposits of oxidized proteins and lipids within the retinal pigment epithelium (RPE). During the visual cycle, RPE supports the photoreceptor cells for the regeneration of visual pigments and breakdown of byproducts. Thus, dysfunction of RPE may result in metabolic burden to the photoreceptor cells. Although the exact cause of AMD is not clear, many studies have indicated that aging, oxidative stress, light damage and genetic factors may play significantly pathogenic roles. Both family and case-control studies revealed that genetic variants at 1q31 and 10q26 are the major genetic contributors. Further functional studies support that complement factor H (CFH) is the main player on chromosome 1q31, while the susceptibility gene on 10q26 remains to be elucidated. The aims of this study are (1) to reconstruct the risk haplotypes at 10q26 in exudative AMD, the prominent form of AMD in Asians strongly associated with the 10q26 variants, and (2) to investigate the role of candidate genes in this region during oxidative stress. Based on meta-analysis of GWAS data from studies of AMD, it was found that the risk locus extends more to the proximal region on 10q26 rather than to the distal region. In addition, due to no consensus on the functional roles for the other two candidates, ARMS2 and HTRA1, we therefore focused on PLEKHA1 as the candidate to investigate its possible role in AMD. So far, we have found that the two major isoforms of PLEKHA1 expressed differently in various tissues and the treatments of hydrogen peroxide, which mimics oxidative stress, induced translocations of PLEKHA1 isoform 1 to the plasma membrane but not isoform 2 in ARPE-19 cells. We further investigated the response of the two isoforms of PLEKHA1 under light exposure in the presence of N-retinyl-N-retinylidene ethanolamine (A2E), an autofluorescent pigment that accumulates in RPE cells in aging and some retinal disorders, which can induce generation of reactive oxygen species and cause serious toxicity to RPE cells. Similarly, A2E oxidative stress could induced translocations of PLEKHA1 isoform 1 to the plasma membrane in ARPE-19 cells. Induced phosphorylation of Akt (v-akt murine thymoma viral oncogen) in ARPE-19 cells under hydrogen peroxide or A2E oxidative stress was observed, but decreased level of phosphorylated Akt were observed in cells overexpressing PLEKHA1 isoform 1 rather than isoform 2. Both hydrogen peroxide and A2E oxidative stress induced cell death in ARPE-19 cells, but overexpressing PLEKHA1 isoform 1 slightly decrease resistance to oxidative stress whereas overexpression of PLEKHA1 isoform 2 slightly increase resistance to oxidative stress. To sum up, PLEKHA1 may play a role in cell survival under oxidative stress, thus it is a putative pathological cause for AMD.
Частини книг з теми "PLEKHO1"
Donato, Dominique M., Steven K. Hanks, Kenneth A. Jacobson, M. P. Suresh Jayasekara, Zhan-Guo Gao, Francesca Deflorian, John Papaconstantinou, et al. "PLEKHO1 (Pleckstrin-Homology Domain Containing, Family O Member 1)." In Encyclopedia of Signaling Molecules, 1446. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_101066.
Повний текст джерелаSpallucci, Euro, Steven Duplij, Anatoly Nikitin, Alexander Galkin, Artur Sergyeyev, Steven Duplij, Omer Faruk Dayi, et al. "Plekton." In Concise Encyclopedia of Supersymmetry, 300. Dordrecht: Springer Netherlands, 2004. http://dx.doi.org/10.1007/1-4020-4522-0_398.
Повний текст джерелаDonato, Dominique M., Steven K. Hanks, Kenneth A. Jacobson, M. P. Suresh Jayasekara, Zhan-Guo Gao, Francesca Deflorian, John Papaconstantinou, et al. "Plekhg5." In Encyclopedia of Signaling Molecules, 1446. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_101065.
Повний текст джерелаHorowitz, Arie. "SYX/PLEKHG5, A Rhoa Guanine Exchange Factor Involved in Cell Migration and Angiogenesis." In Encyclopedia of Signaling Molecules, 5295–98. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_567.
Повний текст джерелаDempsey, Brian R., Anne C. Rintala-Dempsey, Gary S. Shaw, Yuan Xiao Zhu, A. Keith Stewart, Jaime O. Claudio, Constance E. Runyan, et al. "SYX/PLEKHG5, A Rhoa Guanine Exchange Factor Involved in Cell Migration and Angiogenesis." In Encyclopedia of Signaling Molecules, 1827–30. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_567.
Повний текст джерела"PLEKHO1." In Encyclopedia of Signaling Molecules, 4091. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_102971.
Повний текст джерела"Plekhg5." In Encyclopedia of Signaling Molecules, 4091. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_102970.
Повний текст джерелаТези доповідей конференцій з теми "PLEKHO1"
Qian, J., and S. Nan. "307 The pathogenic mechanisms of systemic lupus erythematosus associated genes pnp, plekhf2 and ankrd44." In LUPUS 2017 & ACA 2017, (12th International Congress on SLE &, 7th Asian Congress on Autoimmunity). Lupus Foundation of America, 2017. http://dx.doi.org/10.1136/lupus-2017-000215.307.
Повний текст джерелаJeung, Hei-Cheul, Galina Kiriakova, Lynn Kirkpatrick, Martin Indarte, and Garth Powis. "Abstract A199: The plekstrin-homology-domain-containing protein PLEKHA7 is a novel target for selectively inhibiting mutant KRAS colon cancer cell proliferation." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 12-16, 2011; San Francisco, CA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1535-7163.targ-11-a199.
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