Relevant bibliographies by topics / Interferon-induced transmembrane proteins

Academic literature on the topic 'Interferon-induced transmembrane proteins'

Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Contents

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Interferon-induced transmembrane proteins.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "Interferon-induced transmembrane proteins"

1

Siegrist, Fredy, Martin Ebeling, and Ulrich Certa. "The Small Interferon-Induced Transmembrane Genes and Proteins." Journal of Interferon & Cytokine Research 31, no. 1 (January 2011): 183–97. http://dx.doi.org/10.1089/jir.2010.0112.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Guo, Xiangyang, Jan Steinkühler, Mariana Marin, Rumiana Dimova, and Gregory Melikian. "Inhibition of Viral Fusion by Interferon-Induced Transmembrane Proteins." Biophysical Journal 120, no. 3 (February 2021): 2a. http://dx.doi.org/10.1016/j.bpj.2020.11.093.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Qian, Jin, Yann Le Duff, Yimeng Wang, Qinghua Pan, Shilei Ding, Yi-Min Zheng, Shan-Lu Liu, and Chen Liang. "Primate lentiviruses are differentially inhibited by interferon-induced transmembrane proteins." Virology 474 (January 2015): 10–18. http://dx.doi.org/10.1016/j.virol.2014.10.015.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Zani, Ashley, Lizhi Zhang, Temet M. McMichael, Adam D. Kenney, Mahesh Chemudupati, Jesse J. Kwiek, Shan-Lu Liu, and Jacob S. Yount. "Interferon-induced transmembrane proteins inhibit cell fusion mediated by trophoblast syncytins." Journal of Biological Chemistry 294, no. 52 (November 17, 2019): 19844–51. http://dx.doi.org/10.1074/jbc.ac119.010611.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Hornick, Andrew L., Ni Li, Mayumi Oakland, Paul B. McCray, and Patrick L. Sinn. "Human, Pig, and Mouse Interferon-Induced Transmembrane Proteins Partially Restrict Pseudotyped Lentiviral Vectors." Human Gene Therapy 27, no. 5 (May 2016): 354–62. http://dx.doi.org/10.1089/hum.2015.156.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Buchrieser, Julian, and Olivier Schwartz. "Pregnancy complications and Interferon-induced transmembrane proteins (IFITM): balancing antiviral immunity and placental development." Comptes Rendus. Biologies 344, no. 2 (July 2, 2021): 145–56. http://dx.doi.org/10.5802/crbiol.54.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Narayana, Sumudu K., Karla J. Helbig, Erin M. McCartney, Nicholas S. Eyre, Rowena A. Bull, Auda Eltahla, Andrew R. Lloyd, and Michael R. Beard. "The Interferon-induced Transmembrane Proteins, IFITM1, IFITM2, and IFITM3 Inhibit Hepatitis C Virus Entry." Journal of Biological Chemistry 290, no. 43 (September 9, 2015): 25946–59. http://dx.doi.org/10.1074/jbc.m115.657346.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Sharma, Amit, Richard N. McLaughlin, Ryan S. Basom, Caroline Kikawa, Molly OhAinle, Jacob S. Yount, Michael Emerman, and Julie Overbaugh. "Macaque interferon-induced transmembrane proteins limit replication of SHIV strains in an Envelope-dependent manner." PLOS Pathogens 15, no. 7 (July 1, 2019): e1007925. http://dx.doi.org/10.1371/journal.ppat.1007925.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Xie, Maorong, Baoqin Xuan, Jiaoyu Shan, Deng Pan, Yamei Sun, Zhao Shan, Jinping Zhang, Dong Yu, Bin Li, and Zhikang Qian. "Human Cytomegalovirus Exploits Interferon-Induced Transmembrane Proteins To Facilitate Morphogenesis of the Virion Assembly Compartment." Journal of Virology 89, no. 6 (December 31, 2014): 3049–61. http://dx.doi.org/10.1128/jvi.03416-14.

Full text
Abstract:
ABSTRACTRecently, interferon-induced transmembrane proteins (IFITMs) have been identified to be key effector molecules in the host type I interferon defense system. The invasion of host cells by a large range of RNA viruses is inhibited by IFITMs during the entry step. However, the roles of IFITMs in DNA virus infections have not been studied in detail. In this study, we report that human cytomegalovirus (HCMV), a large human DNA virus, exploits IFITMs to facilitate the formation of the virion assembly compartment (vAC) during infection of human fibroblasts. We found that IFITMs were expressed constitutively in human embryonic lung fibroblasts (MRC5 cells). HCMV infection inhibited IFITM protein accumulation in the later stages of infection. Overexpression of an IFITM protein in MRC5 cells slightly enhanced HCMV production and knockdown of IFITMs by RNA interference reduced the virus titer by about 100-fold on day 8 postinfection, according to the findings of a virus yield assay at a low multiplicity of infection. Virus gene expression and DNA synthesis were not affected, but the typical round structure of the vAC was not formed after the suppression of IFITMs, thereby resulting in defective virion assembly and the production of less infectious virion particles. Interestingly, the replication of herpes simplex virus, a human herpesvirus that is closely related to HCMV, was not affected by the suppression of IFITMs in MRC5 cells. These results indicate that IFITMs are involved in a specific pathway required for HCMV replication.IMPORTANCEHCMV is known to repurpose the interferon-stimulated genes (ISGs) viperin and tetherin to facilitate its replication. Our results expand the range of ISGs that can be exploited by HCMV for its replication. This is also the first report of a proviral function of IFITMs in DNA virus replication. In addition, whereas previous studies showed that IFITMs modulate virus entry, which is a very early stage in the virus life cycle, we identified a new function of IFITMs during the very late stage of virus replication, i.e., virion assembly. Virus entry and assembly both involve vesicle transport and membrane fusion; thus, a common biochemical activity of IFITMs is likely to be involved. Therefore, our findings may provide a new platform for dissecting the molecular mechanism of action of IFITMs during the blocking or enhancement of virus infection, which are under intense investigation in this field.
APA, Harvard, Vancouver, ISO, and other styles
10

Wrensch, Florian, Gaëtan Ligat, Laura Heydmann, Catherine Schuster, Mirjam B. Zeisel, Patrick Pessaux, François Habersetzer, et al. "Interferon‐Induced Transmembrane Proteins Mediate Viral Evasion in Acute and Chronic Hepatitis C Virus Infection." Hepatology 70, no. 5 (June 21, 2019): 1506–20. http://dx.doi.org/10.1002/hep.30699.

Full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "Interferon-induced transmembrane proteins"

1

Lu, Jennifer. "Interferon-induced transmembrane proteins inhibit human immunodeficiency virus type 1 replication." Thesis, McGill University, 2010. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=95120.

Full text
Abstract:
Viral infection triggers production of interferon (IFN) that in turn leads to the expression of genes known as IFN-stimulated genes (ISGs), some of which possess antiviral activities. Previous studies have shown that IFN suppresses the replication of human immunodeficiency virus type I (HIV-1). While several ISGs have been linked to this specific antiviral activity with well-defined inhibitory mechanisms, others remain to be investigated. With the purpose of identifying novel ISGs capable of inhibiting HIV-1 replication, we have performed a shRNA screen of the genes upregulated by IFN in SupT1 cells. This study reports three ISGs, known as interferon-induced transmembrane proteins 1, 2 and 3 (IFITM1, 2 and 3), that substantially inhibit HIV-1 replication in SupT1 cells. Further studies suggest that HIV-1 entry is impaired. Collectively, these findings identify a small family of cellular restriction factors that serve as a barrier to HIV-1 entry into the host cell.
Suite à une infection virale, les interférons (IFNs) sont produites et servent à induire l'expression de certains gènes, appelés gènes stimulés par l'interféron (ISGs), dont certains possèdent des effets antivirales. Plusieurs études ont démontré que l'IFN possède la capacité d'inhiber la réplication virale du virus de l'immunodéficience humaine de type I (VIH-1). Tandis que certains ISGs ont été associés à une activité antivirale spécifique avec un mécanisme d'action bien défini, d'autres ISGs sont moins bien caractérisés. Dans le but d'identifier de nouveaux ISGs responsables d'inhiber la réplication virale du VIH-1, nous avons réalisé un criblage par shRNA des gènes régulés par l'IFN dans les cellules SupT1. Cette étude rapporte trois ISGs, appelés «interferon-induced transmembrane proteins 1, 2 et 3» (IFITM1, 2, et 3), dont l'expression dans les cellules SupT1 peut inhiber la réplication virale du VIH-1 de façon significative. Les résultats indiquent que ces protéines agissent au niveau de l'entrée du virus dans la cellule. Collectivement, cette étude a identifié une famille de facteur de restriction cellulaire qui agit comme barrière pour prévenir l'entrée du VIH-1 dans la cellule hôte.
APA, Harvard, Vancouver, ISO, and other styles
2

Yu, Fang, and 喻芳. "Functional characterization of interferon induced transmembrane protein-1 in colorectal cancer and glioma carcinogenesis." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B46079956.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

McMichael, Temet M. "Posttranslational modifications and virus restriction activity of IFITM3." The Ohio State University, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=osu1531146508041228.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Narayana, Sumudu Kumari. "Defining and characterising the anti-HCV actions of the interferon-induced transmembrane proteins." Thesis, 2015. http://hdl.handle.net/2440/98685.

Full text
Abstract:
Hepatitis C virus (HCV) is a significant human pathogen of the liver that in the majority of infected individuals causes a chronic infection of the liver. This may over time culminate in the development of severe liver disease such as cirrhosis and hepatocellular carcinoma. Prior to 2012, the only treatment option available for HCV infection was combination therapy with pegylated interferon-α (IFN-α) and ribavirin. However, the recent development and addition of direct acting antivirals (DAAs) into treatment regimes has significantly improved sustained virological response rates. While the ultimate aim is for IFN-α free therapy, IFN-α is often required in combination with the DAAs to reduce the development of viral resistance and due to cost. It is clear that IFN (either exogenous or endogenous) can induce an antiviral state in HCV infected cells; however, the exact mechanisms that underpin this action remain unclear. The interferon-induced transmembrane (IFITM) family of proteins - IFITM1, IFITM2 and IFITM3 has recently been identified as important host effector molecules of the type I IFN response against a broad range of RNA viruses. During the course of this PhD study, a number of investigations identified the IFITM proteins to be potent antiviral effectors against HCV; however, the mechanism(s) for this antiviral activity remains contradictory. In this thesis, we demonstrate that IFITM1, IFITM2 and IFITM3 play an integral role in the IFN response against HCV and act specifically to inhibit early and late stages of HCV entry to inhibit infection. We reveal that IFITM1 localises to the cell surface in hepatocytes and interacts with the host entry factor CD81 to limit HCV entry. Furthermore, the N-terminus, in particular amino acids 21-28, of IFITM1 plays an important role in this anti-HCV activity, while the C-terminus is found to be important for localisation to the cell surface. We also established that in hepatocytes, IFITM2 and IFITM3 localise to the late and early endosomes respectively, as well as the lysosome, indicating that IFITM2 and IFITM3 follow the established paradigm of targeting the late entry stages of HCV infection. Furthermore, we have demonstrated that S-palmitoylation of all three IFITM proteins is essential for both anti-HCV activity and cellular localisation, while the conserved tyrosine residue in the N-terminus of IFITM2 and IFITM3 plays a significant role in protein localisation. However, this tyrosine was found to be dispensable for anti-HCV activity, with mutation of the tyrosine resulting in an IFITM1-like phenotype with the retention of anti-HCV activity and co-localisation of IFITM2 and IFITM3 with CD81. In conclusion, we propose that the IFITM proteins act in a coordinated manner to restrict HCV infection by targeting the endocytosed HCV virion for lysosomal degradation and demonstrate that the actions of the IFITM proteins are indeed virus and cell-type specific. We believe we have significantly added to our understanding of the interplay between HCV and the host innate immune response and that in the long term these findings will aid in the generation of novel and targeted anti-HCV therapeutics for patients chronically infected with HCV.
Thesis (Ph.D.) -- University of Adelaide, School of Biological Sciences, 2015.
APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "Interferon-induced transmembrane proteins"

1

Ogony, Joshua W., and Joan Lewis-Wambi. "Abstract 4617: Targeting interferon-induced transmembrane protein 1: a novel strategy to treat inflammatory breast cancer." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-4617.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Provance, Olivia, Eric Geanes, Joshua Ogony, Asona Lui, Eric Young, Sumedha Gunewardena, and Joan Lewis-Wambi. "Abstract 1899: Targeting interferon induced transmembrane protein-1 (IFITM1) attenuates the aggressive phenotype of inflammatory breast cancer." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-1899.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Choi, Hye Joung, and Joan Lewis-Wambi. "Abstract 25: Loss of interferon-induced transmembrane protein 1 enhances estrogen-induced cell death in AI-resistant breast cancer cells." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-25.

Full text
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'Interferon-induced transmembrane proteins' for particular source types:
Journal articles
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography