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Search results 301 to 317 out of 317 for Fgg

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Type Details Score
Publication
First Author: Lord ST
Year: 1990
Journal: J Biol Chem
Title: Analysis of fibrinogen A alpha-fusion proteins. Mutants which inhibit thrombin equivalently are not equally good substrates.
Volume: 265
Issue: 2
Pages: 838-43
Publication
First Author: Kirschbaum NE
Year: 1990
Journal: J Biol Chem
Title: A unique proteolytic fragment of human fibrinogen containing the A alpha COOH-terminal domain of the native molecule.
Volume: 265
Issue: 23
Pages: 13669-76
Publication
First Author: Ghosh S
Year: 2020
Journal: Cell
Title: β-Coronaviruses Use Lysosomes for Egress Instead of the Biosynthetic Secretory Pathway.
Volume: 183
Issue: 6
Pages: 1520-1535.e14
Publication
First Author: Tan YJ
Year: 2005
Journal: J Virol
Title: The severe acute respiratory syndrome coronavirus 3a protein up-regulates expression of fibrinogen in lung epithelial cells.
Volume: 79
Issue: 15
Pages: 10083-7
Publication
First Author: Oostra M
Year: 2006
Journal: J Virol
Title: Glycosylation of the severe acute respiratory syndrome coronavirus triple-spanning membrane proteins 3a and M.
Volume: 80
Issue: 5
Pages: 2326-36
Publication
First Author: Lu W
Year: 2006
Journal: Proc Natl Acad Sci U S A
Title: Severe acute respiratory syndrome-associated coronavirus 3a protein forms an ion channel and modulates virus release.
Volume: 103
Issue: 33
Pages: 12540-5
Publication
First Author: Yu CJ
Year: 2004
Journal: FEBS Lett
Title: Identification of a novel protein 3a from severe acute respiratory syndrome coronavirus.
Volume: 565
Issue: 1-3
Pages: 111-6
Publication
First Author: Shen S
Year: 2005
Journal: Biochem Biophys Res Commun
Title: The severe acute respiratory syndrome coronavirus 3a is a novel structural protein.
Volume: 330
Issue: 1
Pages: 286-92
Publication
First Author: Minakshi R
Year: 2009
Journal: PLoS One
Title: The SARS Coronavirus 3a protein causes endoplasmic reticulum stress and induces ligand-independent downregulation of the type 1 interferon receptor.
Volume: 4
Issue: 12
Pages: e8342
Publication
First Author: Siu KL
Year: 2019
Journal: FASEB J
Title: Severe acute respiratory syndrome coronavirus ORF3a protein activates the NLRP3 inflammasome by promoting TRAF3-dependent ubiquitination of ASC.
Volume: 33
Issue: 8
Pages: 8865-8877
Publication  
First Author: Farag NS
Year: 2020
Journal: Int J Biochem Cell Biol
Title: Viroporins and inflammasomes: A key to understand virus-induced inflammation.
Volume: 122
Pages: 105738
Publication
First Author: Miao G
Year: 2021
Journal: Dev Cell
Title: ORF3a of the COVID-19 virus SARS-CoV-2 blocks HOPS complex-mediated assembly of the SNARE complex required for autolysosome formation.
Volume: 56
Issue: 4
Pages: 427-442.e5
Publication
First Author: Kern DM
Year: 2021
Journal: Nat Struct Mol Biol
Title: Cryo-EM structure of SARS-CoV-2 ORF3a in lipid nanodiscs.
Volume: 28
Issue: 7
Pages: 573-582
Protein Domain
Type: Family
Description: Coronavirus encodes two viroporins, E protein and protein 3a, which act as ion-conductive pores in planar lipid bilayers and are required for maximal SARS-CoV replication and virulence []. In betacoronavirus, this protein plays a role in viral egress via lysosomal trafficking [, ]. Protein 3a from SARS-CoV-2 also blocks autolysosomes formation by binding and sequestering the host component VPS39 for homotypic fusion and protein sorting (HOPS) on late endosomes. This prevents fusion of autophagosomes with lysosomes, disrupting autophagy and facilitating virus egress [].This entry represents protein 3a encoded by Orf3/3a, also known as X1, which forms homotetrameric potassium, sodium or calcium sensitive ion channels (viroporin) and may modulate virus release. It has also been shown to up-regulate expression of fibrinogen subunits FGA, FGBand FGG in host lung epithelial cells [, , , ].3a protein is a pro-apoptosis-inducing protein. It localises to the endoplasmic reticulum (ER)-Golgi compartment. SARS-CoV causes apoptosis of infected cells through NLRP3 inflammasome activation, as ORF3a is a potent activator of the signals required for this activation, pro-IL-1beta gene transcription and protein maturation. This protein also promotes the ubiquitination of apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC) mediated by its interaction with TNF receptor-associated factor 3 (TRAF3). The expression of ORF3a induces NF-kappa B activation and up-regulates fibrinogen secretion with the consequent high cytokine production [, , , ]. Another apoptosis mechanism described for this protein is the activation of the PERK pathway of unfolded protein response (UPR), which causes phosphorylation of eIF2alpha and leads to reduced translation of cellular proteins as well as the activation of pro-apoptotic downstream effectors (i.e ATF4, CHOP) [].
Protein
Organism: Mus musculus/domesticus
Length: 436  
Fragment?: false
Protein
Organism: Mus musculus/domesticus
Length: 436  
Fragment?: false
Protein
Organism: Mus musculus/domesticus
Length: 443  
Fragment?: false