Relevant bibliographies by topics / Erythropoietin-producing hepatocellular B4 receptor

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  1. Journal articles
  2. Dissertations / Theses
  3. Book chapters

Academic literature on the topic 'Erythropoietin-producing hepatocellular B4 receptor'

Author: Grafiati
Published: 10 January 2023
Last updated: 28 January 2023

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Journal articles on the topic "Erythropoietin-producing hepatocellular B4 receptor"

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Li, Chaohao, Nadia A. Lanman, Yifan Kong, Daheng He, Fengyi Mao, Elia Farah, Yanquan Zhang, et al. "Inhibition of the erythropoietin-producing receptor EPHB4 antagonizes androgen receptor overexpression and reduces enzalutamide resistance." Journal of Biological Chemistry 295, no. 16 (March 17, 2020): 5470–83. http://dx.doi.org/10.1074/jbc.ra119.011385.

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Prostate cancer (PCa) cells heavily rely on an active androgen receptor (AR) pathway for their survival. Enzalutamide (MDV3100) is a second-generation antiandrogenic drug that was approved by the Food and Drug Administration in 2012 to treat patients with castration-resistant prostate cancer (CRPC). However, emergence of resistance against this drug is inevitable, and it has been a major challenge to develop interventions that help manage enzalutamide-resistant CRPC. Erythropoietin-producing human hepatocellular (Eph) receptors are targeted by ephrin protein ligands and have a broad range of functions. Increasing evidence indicates that this signaling pathway plays an important role in tumorigenesis. Overexpression of EPH receptor B4 (EPHB4) has been observed in multiple types of cancer, being closely associated with proliferation, invasion, and metastasis of tumors. Here, using RNA-Seq analyses of clinical and preclinical samples, along with several biochemical and molecular methods, we report that enzalutamide-resistant PCa requires an active EPHB4 pathway that supports drug resistance of this tumor type. Using a small kinase inhibitor and RNAi-based gene silencing to disrupt EPHB4 activity, we found that these disruptions re-sensitize enzalutamide-resistant PCa to the drug both in vitro and in vivo. Mechanistically, we found that EPHB4 stimulates the AR by inducing proto-oncogene c-Myc (c-Myc) expression. Taken together, these results provide critical insight into the mechanism of enzalutamide resistance in PCa, potentially offering a therapeutic avenue for enhancing the efficacy of enzalutamide to better manage this common malignancy.
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Du, Jing, Wei Zhao, Yusheng Wang, and Yan Cai. "Lentivirus Vector-Mediated Knockdown of Erythropoietin-Producing Hepatocellular Carcinoma Receptors B4 Inhibits Laser-Induced Choroidal Neovascularization." Journal of Ocular Pharmacology and Therapeutics 29, no. 1 (February 2013): 14–22. http://dx.doi.org/10.1089/jop.2012.0077.

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Lafleur, Karine, Danzhi Huang, Ting Zhou, Amedeo Caflisch, and Cristina Nevado. "Structure-Based Optimization of Potent and Selective Inhibitors of the Tyrosine Kinase Erythropoietin Producing Human Hepatocellular Carcinoma Receptor B4 (EphB4)." Journal of Medicinal Chemistry 52, no. 20 (October 22, 2009): 6433–46. http://dx.doi.org/10.1021/jm9009444.

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Dong, Ling-Dan, Xiang-Lin Cheng, Long Zhou, Qing Huang, Jun-Chuan Li, and Cun-Jian Yi. "Overexpression of erythropoietin-producing hepatocyte receptor B4 and ephrin-B2 is associated with estrogen receptor expression in endometrial adenocarcinoma." Oncology Letters 13, no. 4 (February 8, 2017): 2109–14. http://dx.doi.org/10.3892/ol.2017.5698.

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Singh, Deo R., QingQing Cao, Christopher King, Matt Salotto, Fozia Ahmed, Xiang Yang Zhou, Elena B. Pasquale, and Kalina Hristova. "Unliganded EphA3 dimerization promoted by the SAM domain." Biochemical Journal 471, no. 1 (September 21, 2015): 101–9. http://dx.doi.org/10.1042/bj20150433.

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Erythropoietin-producing hepatocellular carcinoma A3 (EphA3) can form dimers in the absence of ligand binding, which are stabilized by the sterile α-motif (SAM) domain. This challenges the current understanding of EphA3 activation events and establishes a new role for the EphA3 SAM domain in receptor-receptor interactions.
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Rudzitis‐Auth, Jeannette, Sophia A. Fuß, Vivien Becker, Michael D. Menger, and Matthias W. Laschke. "Inhibition of erythropoietin‐producing hepatoma receptor B4 (EphB4) signalling suppresses the vascularisation and growth of endometriotic lesions." British Journal of Pharmacology 177, no. 14 (April 12, 2020): 3225–39. http://dx.doi.org/10.1111/bph.15044.

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Furukawa, Takenori, Hiroyuki Kimura, Hanae Torimoto, Yusuke Yagi, Hidekazu Kawashima, Kenji Arimitsu, and Hiroyuki Yasui. "A Putative Single-Photon Emission CT Imaging Tracer for Erythropoietin-Producing Hepatocellular A2 Receptor." ACS Medicinal Chemistry Letters 12, no. 8 (July 14, 2021): 1238–44. http://dx.doi.org/10.1021/acsmedchemlett.1c00030.

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Butler, Noah S., and Nathan W. Schmidt. "Erythropoietin-producing hepatocellular receptor B2 receptor tyrosine kinase: A novel regulator of infection- and inflammation-induced liver fibrosis." Hepatology 62, no. 3 (May 26, 2015): 680–83. http://dx.doi.org/10.1002/hep.27868.

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Sun, Chen-Li, Cheng-Wen Li, Nong He, Yuan-Zhang Tang, Xiu-Liang Li, Fu-Shan Xue, and Jia-Xiang Ni. "Blockade of Erythropoietin-Producing Human Hepatocellular Carcinoma Receptor B1 in Spinal Dorsal Horn Alleviates Visceral Pain in Rats." Pain Research and Management 2021 (April 7, 2021): 1–9. http://dx.doi.org/10.1155/2021/7582494.

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Objective. This experiment was designed to determine whether erythropoietin-producing human hepatocellular carcinoma (Eph) receptors were involved in the development of visceral pain. Methods. Adult male Sprague-Dawley rats were randomly divided into three groups receiving different treatments (n = 16 per group): intracolonic vehicle (control group), intracolonic 2, 4, 6-trinitrobenzene sulfonic acid (TNBS) (TNBS group), and intracolonic TNBS and intrathecal EphB1 receptor blocking reagent (TNBS + EphB2-Fc group). Visceral hyperalgesia was evaluated with quantification of visceral pain threshold induced by colorectal distention. The spinal expressions of EphB1 and ephrinB2 and levels of their phosphorylated forms (p-EphB1 and p-ephrinB2) were assessed by Western blotting and immunohistochemistry. Results. The TNBS-treated rats developed significant visceral hyperalgesia. The spinal expressions of EphB1, p-EphB1, ephrinB2, and p-ephrinB2 were significantly increased in the TNBS group compared with the control group, but visceral hyperalgesia and elevation of spinal EphB1 and p-EphB1 expressions were evidently alleviated by intrathecal administration of EphB2-Fc in the TNBS + EphB2-Fc group. The number of EphB1- and p-EphB1-immunopositive cells, the average optical (AO) value of EphB1, and its phosphorylated form in the spinal dorsal horn were significantly increased in the TNBS group than in the control group, but they were obviously reduced by intrathecal administration of EphB2-Fc. There were no significant differences in the number of ephrinB2- and p-ephrinB2-immunopositive cells and the AO value of ephrinB2 and its phosphorylated form between the TNBS and TNBS + EphB2-Fc groups. Conclusion. EphB1 receptors in the spinal dorsal horn play a pivotal role in the development of visceral pain and may be considered as a potential target for the treatment of visceral pain.
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Aasheim, Hans-Christian, Else Munthe, Steinar Funderud, Erlend B. Smeland, Klaus Beiske, and Ton Logtenberg. "A splice variant of human ephrin-A4 encodes a soluble molecule that is secreted by activated human B lymphocytes." Blood 95, no. 1 (January 1, 2000): 221–30. http://dx.doi.org/10.1182/blood.v95.1.221.001k01_221_230.

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Ephrin-A4 is a ligand for the erythropoietin-producing hepatocellular (Eph) receptor family of tyrosine kinases. We have identified a secreted form of ephrin-A4, denoted ephrin-A4 (s), which is encoded by an alternatively spliced mRNA and is produced by in vivo activated B cells in tonsils. Blood B cells secrete ephrin-A4 (s) upon stimulation via the B-cell antigen receptor. A subpopulation of tonsil cells in the crypts with a dendritic cell phenotype was shown to express EphA2, an Eph receptor tyrosine kinase that was found to be capable of binding an ephrin-A4 immunoglobulin chimeric protein. We conclude that ephrin-A4 (s) may play a role in the interaction between activated B lymphocytes and dendritic cells in human tonsils. (Blood. 2000;95:221-230)
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Dissertations / Theses on the topic "Erythropoietin-producing hepatocellular B4 receptor"

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Kadife, Elif. "The Functional and Biological Implications of EphB4 Receptor Overexpression and Knockout in Colorectal Cancer." Thesis, 2018. https://vuir.vu.edu.au/40587/.

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Colorectal cancer (CRC) is one of the most frequently diagnosed cancers in Australia and globally. Early detection and intervention is vital for the longevity of patients with any cancer, however, this appears to be most challenging with CRC, as it is largely asymptomatic. For this reason, most cases are not diagnosed until the cancer has metastasised, primarily to the liver. At this late stage of diagnosis, 5- year patient’s survival is predicted to be less than 10%. However, even when CRC is diagnosed and treated in the initial stages of neoplastic growth, high recurrence rates in patients still present as a serious issue. The problems associated with treatment and recurrence raise the need to identify molecular targets, so that specific and aggressive therapeutic interventions may be designed and developed. One such potential target is the erythropoietin-producing hepatocellular B4 (EphB4) receptor. The Ephs constitute the largest family of tyrosine kinase receptors. The activation of Eph receptors is achieved through association with their corresponding cell- bound ‘Eph receptor interacting’ (Ephrin) ligands. The signalling by the Eph receptors and their membrane-bound ligands, the Ephrins, is unique among the tyrosine kinases as both the receptor and ligand are found on the cell surface. Bidirectional interaction results in the phenomena of ‘forward’ signalling via the Eph receptor carrying cells and ‘reverse’ signalling in those cells expressing the Ephrin ligands. Several members of the Eph receptor receptor family, including EphB4, have been implicated with progression of many different types of cancer. However, EphB4 receptor’s contribution towards CRC yields the most contradictory findings. Some studies suggest that EphB4 is upregulated in late and metastatic stages of CRC, while others argue that EphB4 expression is often silenced in the progressive state of the disease. Due to the promising results achieved in other types of cancers, it is important to elucidate the role of EphB4 receptors in CRC in order to develop more specific and aggressive cancer therapies. The overall aim of this study is to elucidate the influence of EphB4 receptor expression on the development and progression of CRC. To achieve this, we used modified derivatives of multiple human and a mouse CRC cell line in in vitro and in vivo experiments. In vitro experiments were utilised to study effects of EphB4 overexpression and knockout on proliferative aptitude, migratory and invasive abilities of human and mouse CRC cells. In vivo subcutaneous models of CRC were used to evaluate the ability of high, low and knockdown of EphB4 receptor expression to influence morphological changes, rate of growth, vascularization and tumour-stromal interactions. The time course and rate of metastasis of CRC cells to the liver were studied in in vivo orthotopic and intra-splenic metastasis models. The level of EPHB4 and EPHRINB2 expression was investigated using databases to determine their correlation with survival and disease-free outcomes of CRC patients. The results of this study provide evidence that high EphB4 receptor expression significantly increases the rate of proliferation, migration and invasion of CRC cells in vitro, and enhances tumour growth in vivo due to enhanced vascularisation. Knockout of EphB4 expression reduces these effects. EphrinB2 appears to inhibit proliferation in cells overexpressing EphB4 and its expression correlates with poor patient outcome.
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Book chapters on the topic "Erythropoietin-producing hepatocellular B4 receptor"

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Salajegheh, Ali. "Erythropoietin-Producing Hepatocellular Receptors B: Ephrin B2, Ephrin B4." In Angiogenesis in Health, Disease and Malignancy, 89–96. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-28140-7_15.

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Zhou, Renping. "EphA3, Erythropoietin-Producing Hepatocellular Carcinoma Cell Receptor A3." In Encyclopedia of Signaling Molecules, 1573–81. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_628.

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Miki, Toru, Randa Hilal-Dandan, Laurence L. Brunton, Jean Sévigny, Kwok-On Lai, Nancy Y. Ip, Renping Zhou, et al. "EphA3, Erythropoietin-Producing Hepatocellular Carcinoma Cell Receptor A3." In Encyclopedia of Signaling Molecules, 567–73. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_628.

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Journal articles
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