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unc93b1 protein  (Fukui Bank Ltd)

 
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    Structured Review

    Fukui Bank Ltd unc93b1 protein
    Unc93b1 Protein, supplied by Fukui Bank Ltd, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/unc93b1+protein/unc93b1+protein/pm39961973-158-0-16
    Average 90 stars, based on 1 article reviews
    unc93b1 protein - by Bioz Stars, 2026-10
    90/100 stars

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    Related Articles

    Derivative Assay:

    Article Title: Unc93b1 is essential for cytokine activation of five PAMPs in the orange-spotted grouper (Epinephelus coioides).
    Article Snippet: 19 Toll-like receptors (TLRs) are important innate immune receptors that recognize 20 multiple pathogen-associated molecular patterns (PAMPs) and activate the immune 21 responses to resist the invasion of pathogens.. Many TLRs need assistance from 22 trafficking chaperones to transport to the specific cell compartments and then are 23 processed before they are activated.. In this study, we identified an important 24 trafficking chaperone, UNC93 homologue B1 (unc93b1), from the Epinephelus 25 coioides (orange-spotted grouper).

    Article Title: Toll-like Receptors in the Vascular System: Sensing the Dangers Within
    Article Snippet: UNC93B1 also regulates excessive TLR7 signaling by recruiting TLR9 to counteract TLR7 ( Fukui et al., 2009 ).

    Article Title: Toll-like receptor signaling in teleosts.
    Article Snippet: Toll-like receptors (TLRs) sit at the top of the immune system pyramid.. They form a paramount family of immune sentinels capable of sensing diverse microbe-associated molecular patterns (MAPMs), danger/damage-associated molecular patterns (DAMPs), and other signals.. These perceptions trigger immediate innate immunity and instruct subsequent adaptive immunity.

    Article Title: Microbial Sensing by Toll-Like Receptors and Intracellular Nucleic Acid Sensors
    Article Snippet: Further, UNC93B1 actively and continuously regulates excessive TLR7 activation of immune cells by using TLR9 to counteract TLR7 as shown by mice harboring an amino acid substitution (D34 to A) in UNC93B1, that shows TLR7-hyperreactive and TLR9-hyporeactive phenotype and subsequent TLR7-dependent systemic lethal inflammation, thereby supporting the understanding that an opposing relationship between TLR7 and TLR9 is a potential mechanism regulating autoimmunity ( Fukui et al. 2011 ).

    Article Title: Human antimicrobial peptides in ocular surface defense.
    Article Snippet: Mice deficient in UNC93B1, an essential protein that is required for TLR3, TLR7 923 and TLR9 activation, are highly susceptible to infection with T. cruzi (Caetano et al., 924 2011; Fukui et al., 2009).

    Article Title: The Chaperone UNC93B1 Regulates Toll-like Receptor Stability Independently of Endosomal TLR Transport.
    Article Snippet: Second, UNC93B1 has been shown to act as a key regulator of NA-sensing TLRs (Fukui et al., 2011; Fukui et al., 2009).

    Article Title: Gain-of-function human UNC93B1 variants cause systemic lupus erythematosus and chilblain lupus.
    Article Snippet: Mouse UNC93B1 is best known for mediating TLR signaling through the trafficking of TLR3, 7, and 9 (Kim et al., 2008; Fukui et al., 2011; Majer et al., 2019a, 2019b).

    Article Title: The Chaperone UNC93B1 Regulates Toll-like Receptor Stability Independently of Endosomal TLR Transport.
    Article Snippet: Various studies in mouse also suggest a regulatory function of UNC93B1 in the fine-tuning of NA-sensing TLR responses (Fukui et al., 2009; Lee et al., 2013) and show that dysregulation at the level of UNC93B1 leads to autoinflammatory diseases (Fukui et al., 2011).

    Binding Assay:

    Article Title: Unc93b1 is essential for cytokine activation of five PAMPs in the orange-spotted grouper (Epinephelus coioides).
    Article Snippet: 19 Toll-like receptors (TLRs) are important innate immune receptors that recognize 20 multiple pathogen-associated molecular patterns (PAMPs) and activate the immune 21 responses to resist the invasion of pathogens.. Many TLRs need assistance from 22 trafficking chaperones to transport to the specific cell compartments and then are 23 processed before they are activated.. In this study, we identified an important 24 trafficking chaperone, UNC93 homologue B1 (unc93b1), from the Epinephelus 25 coioides (orange-spotted grouper).

    Article Title: Toll-like Receptors in the Vascular System: Sensing the Dangers Within
    Article Snippet: UNC93B1 also regulates excessive TLR7 signaling by recruiting TLR9 to counteract TLR7 ( Fukui et al., 2009 ).

    Article Title: Toll-like receptor signaling in teleosts.
    Article Snippet: Toll-like receptors (TLRs) sit at the top of the immune system pyramid.. They form a paramount family of immune sentinels capable of sensing diverse microbe-associated molecular patterns (MAPMs), danger/damage-associated molecular patterns (DAMPs), and other signals.. These perceptions trigger immediate innate immunity and instruct subsequent adaptive immunity.

    Article Title: Microbial Sensing by Toll-Like Receptors and Intracellular Nucleic Acid Sensors
    Article Snippet: Further, UNC93B1 actively and continuously regulates excessive TLR7 activation of immune cells by using TLR9 to counteract TLR7 as shown by mice harboring an amino acid substitution (D34 to A) in UNC93B1, that shows TLR7-hyperreactive and TLR9-hyporeactive phenotype and subsequent TLR7-dependent systemic lethal inflammation, thereby supporting the understanding that an opposing relationship between TLR7 and TLR9 is a potential mechanism regulating autoimmunity ( Fukui et al. 2011 ).

    Article Title: Human antimicrobial peptides in ocular surface defense.
    Article Snippet: Mice deficient in UNC93B1, an essential protein that is required for TLR3, TLR7 923 and TLR9 activation, are highly susceptible to infection with T. cruzi (Caetano et al., 924 2011; Fukui et al., 2009).

    Article Title: The Chaperone UNC93B1 Regulates Toll-like Receptor Stability Independently of Endosomal TLR Transport.
    Article Snippet: Second, UNC93B1 has been shown to act as a key regulator of NA-sensing TLRs (Fukui et al., 2011; Fukui et al., 2009).

    Article Title: Gain-of-function human UNC93B1 variants cause systemic lupus erythematosus and chilblain lupus.
    Article Snippet: Mouse UNC93B1 is best known for mediating TLR signaling through the trafficking of TLR3, 7, and 9 (Kim et al., 2008; Fukui et al., 2011; Majer et al., 2019a, 2019b).

    Article Title: The Chaperone UNC93B1 Regulates Toll-like Receptor Stability Independently of Endosomal TLR Transport.
    Article Snippet: Various studies in mouse also suggest a regulatory function of UNC93B1 in the fine-tuning of NA-sensing TLR responses (Fukui et al., 2009; Lee et al., 2013) and show that dysregulation at the level of UNC93B1 leads to autoinflammatory diseases (Fukui et al., 2011).

    Expressing:

    Article Title: Unc93b1 is essential for cytokine activation of five PAMPs in the orange-spotted grouper (Epinephelus coioides).
    Article Snippet: 19 Toll-like receptors (TLRs) are important innate immune receptors that recognize 20 multiple pathogen-associated molecular patterns (PAMPs) and activate the immune 21 responses to resist the invasion of pathogens.. Many TLRs need assistance from 22 trafficking chaperones to transport to the specific cell compartments and then are 23 processed before they are activated.. In this study, we identified an important 24 trafficking chaperone, UNC93 homologue B1 (unc93b1), from the Epinephelus 25 coioides (orange-spotted grouper).

    Article Title: Toll-like Receptors in the Vascular System: Sensing the Dangers Within
    Article Snippet: UNC93B1 also regulates excessive TLR7 signaling by recruiting TLR9 to counteract TLR7 ( Fukui et al., 2009 ).

    Article Title: Toll-like receptor signaling in teleosts.
    Article Snippet: Toll-like receptors (TLRs) sit at the top of the immune system pyramid.. They form a paramount family of immune sentinels capable of sensing diverse microbe-associated molecular patterns (MAPMs), danger/damage-associated molecular patterns (DAMPs), and other signals.. These perceptions trigger immediate innate immunity and instruct subsequent adaptive immunity.

    Article Title: Microbial Sensing by Toll-Like Receptors and Intracellular Nucleic Acid Sensors
    Article Snippet: Further, UNC93B1 actively and continuously regulates excessive TLR7 activation of immune cells by using TLR9 to counteract TLR7 as shown by mice harboring an amino acid substitution (D34 to A) in UNC93B1, that shows TLR7-hyperreactive and TLR9-hyporeactive phenotype and subsequent TLR7-dependent systemic lethal inflammation, thereby supporting the understanding that an opposing relationship between TLR7 and TLR9 is a potential mechanism regulating autoimmunity ( Fukui et al. 2011 ).

    Article Title: Human antimicrobial peptides in ocular surface defense.
    Article Snippet: Mice deficient in UNC93B1, an essential protein that is required for TLR3, TLR7 923 and TLR9 activation, are highly susceptible to infection with T. cruzi (Caetano et al., 924 2011; Fukui et al., 2009).

    Article Title: The Chaperone UNC93B1 Regulates Toll-like Receptor Stability Independently of Endosomal TLR Transport.
    Article Snippet: Second, UNC93B1 has been shown to act as a key regulator of NA-sensing TLRs (Fukui et al., 2011; Fukui et al., 2009).

    Article Title: Gain-of-function human UNC93B1 variants cause systemic lupus erythematosus and chilblain lupus.
    Article Snippet: Mouse UNC93B1 is best known for mediating TLR signaling through the trafficking of TLR3, 7, and 9 (Kim et al., 2008; Fukui et al., 2011; Majer et al., 2019a, 2019b).

    Article Title: The Chaperone UNC93B1 Regulates Toll-like Receptor Stability Independently of Endosomal TLR Transport.
    Article Snippet: Various studies in mouse also suggest a regulatory function of UNC93B1 in the fine-tuning of NA-sensing TLR responses (Fukui et al., 2009; Lee et al., 2013) and show that dysregulation at the level of UNC93B1 leads to autoinflammatory diseases (Fukui et al., 2011).

    Recombinant:

    Article Title: Unc93b1 is essential for cytokine activation of five PAMPs in the orange-spotted grouper (Epinephelus coioides).
    Article Snippet: 19 Toll-like receptors (TLRs) are important innate immune receptors that recognize 20 multiple pathogen-associated molecular patterns (PAMPs) and activate the immune 21 responses to resist the invasion of pathogens.. Many TLRs need assistance from 22 trafficking chaperones to transport to the specific cell compartments and then are 23 processed before they are activated.. In this study, we identified an important 24 trafficking chaperone, UNC93 homologue B1 (unc93b1), from the Epinephelus 25 coioides (orange-spotted grouper).

    Article Title: Toll-like Receptors in the Vascular System: Sensing the Dangers Within
    Article Snippet: UNC93B1 also regulates excessive TLR7 signaling by recruiting TLR9 to counteract TLR7 ( Fukui et al., 2009 ).

    Article Title: Toll-like receptor signaling in teleosts.
    Article Snippet: Toll-like receptors (TLRs) sit at the top of the immune system pyramid.. They form a paramount family of immune sentinels capable of sensing diverse microbe-associated molecular patterns (MAPMs), danger/damage-associated molecular patterns (DAMPs), and other signals.. These perceptions trigger immediate innate immunity and instruct subsequent adaptive immunity.

    Article Title: Microbial Sensing by Toll-Like Receptors and Intracellular Nucleic Acid Sensors
    Article Snippet: Further, UNC93B1 actively and continuously regulates excessive TLR7 activation of immune cells by using TLR9 to counteract TLR7 as shown by mice harboring an amino acid substitution (D34 to A) in UNC93B1, that shows TLR7-hyperreactive and TLR9-hyporeactive phenotype and subsequent TLR7-dependent systemic lethal inflammation, thereby supporting the understanding that an opposing relationship between TLR7 and TLR9 is a potential mechanism regulating autoimmunity ( Fukui et al. 2011 ).

    Article Title: Human antimicrobial peptides in ocular surface defense.
    Article Snippet: Mice deficient in UNC93B1, an essential protein that is required for TLR3, TLR7 923 and TLR9 activation, are highly susceptible to infection with T. cruzi (Caetano et al., 924 2011; Fukui et al., 2009).

    Article Title: The Chaperone UNC93B1 Regulates Toll-like Receptor Stability Independently of Endosomal TLR Transport.
    Article Snippet: Second, UNC93B1 has been shown to act as a key regulator of NA-sensing TLRs (Fukui et al., 2011; Fukui et al., 2009).

    Article Title: Gain-of-function human UNC93B1 variants cause systemic lupus erythematosus and chilblain lupus.
    Article Snippet: Mouse UNC93B1 is best known for mediating TLR signaling through the trafficking of TLR3, 7, and 9 (Kim et al., 2008; Fukui et al., 2011; Majer et al., 2019a, 2019b).

    Article Title: The Chaperone UNC93B1 Regulates Toll-like Receptor Stability Independently of Endosomal TLR Transport.
    Article Snippet: Various studies in mouse also suggest a regulatory function of UNC93B1 in the fine-tuning of NA-sensing TLR responses (Fukui et al., 2009; Lee et al., 2013) and show that dysregulation at the level of UNC93B1 leads to autoinflammatory diseases (Fukui et al., 2011).

    Retroviral:

    Article Title: Unc93b1 is essential for cytokine activation of five PAMPs in the orange-spotted grouper (Epinephelus coioides).
    Article Snippet: 19 Toll-like receptors (TLRs) are important innate immune receptors that recognize 20 multiple pathogen-associated molecular patterns (PAMPs) and activate the immune 21 responses to resist the invasion of pathogens.. Many TLRs need assistance from 22 trafficking chaperones to transport to the specific cell compartments and then are 23 processed before they are activated.. In this study, we identified an important 24 trafficking chaperone, UNC93 homologue B1 (unc93b1), from the Epinephelus 25 coioides (orange-spotted grouper).

    Article Title: Toll-like Receptors in the Vascular System: Sensing the Dangers Within
    Article Snippet: UNC93B1 also regulates excessive TLR7 signaling by recruiting TLR9 to counteract TLR7 ( Fukui et al., 2009 ).

    Article Title: Toll-like receptor signaling in teleosts.
    Article Snippet: Toll-like receptors (TLRs) sit at the top of the immune system pyramid.. They form a paramount family of immune sentinels capable of sensing diverse microbe-associated molecular patterns (MAPMs), danger/damage-associated molecular patterns (DAMPs), and other signals.. These perceptions trigger immediate innate immunity and instruct subsequent adaptive immunity.

    Article Title: Microbial Sensing by Toll-Like Receptors and Intracellular Nucleic Acid Sensors
    Article Snippet: Further, UNC93B1 actively and continuously regulates excessive TLR7 activation of immune cells by using TLR9 to counteract TLR7 as shown by mice harboring an amino acid substitution (D34 to A) in UNC93B1, that shows TLR7-hyperreactive and TLR9-hyporeactive phenotype and subsequent TLR7-dependent systemic lethal inflammation, thereby supporting the understanding that an opposing relationship between TLR7 and TLR9 is a potential mechanism regulating autoimmunity ( Fukui et al. 2011 ).

    Article Title: Human antimicrobial peptides in ocular surface defense.
    Article Snippet: Mice deficient in UNC93B1, an essential protein that is required for TLR3, TLR7 923 and TLR9 activation, are highly susceptible to infection with T. cruzi (Caetano et al., 924 2011; Fukui et al., 2009).

    Article Title: The Chaperone UNC93B1 Regulates Toll-like Receptor Stability Independently of Endosomal TLR Transport.
    Article Snippet: Second, UNC93B1 has been shown to act as a key regulator of NA-sensing TLRs (Fukui et al., 2011; Fukui et al., 2009).

    Article Title: Gain-of-function human UNC93B1 variants cause systemic lupus erythematosus and chilblain lupus.
    Article Snippet: Mouse UNC93B1 is best known for mediating TLR signaling through the trafficking of TLR3, 7, and 9 (Kim et al., 2008; Fukui et al., 2011; Majer et al., 2019a, 2019b).

    Article Title: The Chaperone UNC93B1 Regulates Toll-like Receptor Stability Independently of Endosomal TLR Transport.
    Article Snippet: Various studies in mouse also suggest a regulatory function of UNC93B1 in the fine-tuning of NA-sensing TLR responses (Fukui et al., 2009; Lee et al., 2013) and show that dysregulation at the level of UNC93B1 leads to autoinflammatory diseases (Fukui et al., 2011).

    Transduction:

    Article Title: Unc93b1 is essential for cytokine activation of five PAMPs in the orange-spotted grouper (Epinephelus coioides).
    Article Snippet: 19 Toll-like receptors (TLRs) are important innate immune receptors that recognize 20 multiple pathogen-associated molecular patterns (PAMPs) and activate the immune 21 responses to resist the invasion of pathogens.. Many TLRs need assistance from 22 trafficking chaperones to transport to the specific cell compartments and then are 23 processed before they are activated.. In this study, we identified an important 24 trafficking chaperone, UNC93 homologue B1 (unc93b1), from the Epinephelus 25 coioides (orange-spotted grouper).

    Article Title: Toll-like Receptors in the Vascular System: Sensing the Dangers Within
    Article Snippet: UNC93B1 also regulates excessive TLR7 signaling by recruiting TLR9 to counteract TLR7 ( Fukui et al., 2009 ).

    Article Title: Toll-like receptor signaling in teleosts.
    Article Snippet: Toll-like receptors (TLRs) sit at the top of the immune system pyramid.. They form a paramount family of immune sentinels capable of sensing diverse microbe-associated molecular patterns (MAPMs), danger/damage-associated molecular patterns (DAMPs), and other signals.. These perceptions trigger immediate innate immunity and instruct subsequent adaptive immunity.

    Article Title: Microbial Sensing by Toll-Like Receptors and Intracellular Nucleic Acid Sensors
    Article Snippet: Further, UNC93B1 actively and continuously regulates excessive TLR7 activation of immune cells by using TLR9 to counteract TLR7 as shown by mice harboring an amino acid substitution (D34 to A) in UNC93B1, that shows TLR7-hyperreactive and TLR9-hyporeactive phenotype and subsequent TLR7-dependent systemic lethal inflammation, thereby supporting the understanding that an opposing relationship between TLR7 and TLR9 is a potential mechanism regulating autoimmunity ( Fukui et al. 2011 ).

    Article Title: Human antimicrobial peptides in ocular surface defense.
    Article Snippet: Mice deficient in UNC93B1, an essential protein that is required for TLR3, TLR7 923 and TLR9 activation, are highly susceptible to infection with T. cruzi (Caetano et al., 924 2011; Fukui et al., 2009).

    Article Title: The Chaperone UNC93B1 Regulates Toll-like Receptor Stability Independently of Endosomal TLR Transport.
    Article Snippet: Second, UNC93B1 has been shown to act as a key regulator of NA-sensing TLRs (Fukui et al., 2011; Fukui et al., 2009).

    Article Title: Gain-of-function human UNC93B1 variants cause systemic lupus erythematosus and chilblain lupus.
    Article Snippet: Mouse UNC93B1 is best known for mediating TLR signaling through the trafficking of TLR3, 7, and 9 (Kim et al., 2008; Fukui et al., 2011; Majer et al., 2019a, 2019b).

    Article Title: The Chaperone UNC93B1 Regulates Toll-like Receptor Stability Independently of Endosomal TLR Transport.
    Article Snippet: Various studies in mouse also suggest a regulatory function of UNC93B1 in the fine-tuning of NA-sensing TLR responses (Fukui et al., 2009; Lee et al., 2013) and show that dysregulation at the level of UNC93B1 leads to autoinflammatory diseases (Fukui et al., 2011).

    Software:

    Article Title: Unc93b1 is essential for cytokine activation of five PAMPs in the orange-spotted grouper (Epinephelus coioides).
    Article Snippet: 19 Toll-like receptors (TLRs) are important innate immune receptors that recognize 20 multiple pathogen-associated molecular patterns (PAMPs) and activate the immune 21 responses to resist the invasion of pathogens.. Many TLRs need assistance from 22 trafficking chaperones to transport to the specific cell compartments and then are 23 processed before they are activated.. In this study, we identified an important 24 trafficking chaperone, UNC93 homologue B1 (unc93b1), from the Epinephelus 25 coioides (orange-spotted grouper).

    Article Title: Toll-like Receptors in the Vascular System: Sensing the Dangers Within
    Article Snippet: UNC93B1 also regulates excessive TLR7 signaling by recruiting TLR9 to counteract TLR7 ( Fukui et al., 2009 ).

    Article Title: Toll-like receptor signaling in teleosts.
    Article Snippet: Toll-like receptors (TLRs) sit at the top of the immune system pyramid.. They form a paramount family of immune sentinels capable of sensing diverse microbe-associated molecular patterns (MAPMs), danger/damage-associated molecular patterns (DAMPs), and other signals.. These perceptions trigger immediate innate immunity and instruct subsequent adaptive immunity.

    Article Title: Microbial Sensing by Toll-Like Receptors and Intracellular Nucleic Acid Sensors
    Article Snippet: Further, UNC93B1 actively and continuously regulates excessive TLR7 activation of immune cells by using TLR9 to counteract TLR7 as shown by mice harboring an amino acid substitution (D34 to A) in UNC93B1, that shows TLR7-hyperreactive and TLR9-hyporeactive phenotype and subsequent TLR7-dependent systemic lethal inflammation, thereby supporting the understanding that an opposing relationship between TLR7 and TLR9 is a potential mechanism regulating autoimmunity ( Fukui et al. 2011 ).

    Article Title: Human antimicrobial peptides in ocular surface defense.
    Article Snippet: Mice deficient in UNC93B1, an essential protein that is required for TLR3, TLR7 923 and TLR9 activation, are highly susceptible to infection with T. cruzi (Caetano et al., 924 2011; Fukui et al., 2009).

    Article Title: The Chaperone UNC93B1 Regulates Toll-like Receptor Stability Independently of Endosomal TLR Transport.
    Article Snippet: Second, UNC93B1 has been shown to act as a key regulator of NA-sensing TLRs (Fukui et al., 2011; Fukui et al., 2009).

    Article Title: Gain-of-function human UNC93B1 variants cause systemic lupus erythematosus and chilblain lupus.
    Article Snippet: Mouse UNC93B1 is best known for mediating TLR signaling through the trafficking of TLR3, 7, and 9 (Kim et al., 2008; Fukui et al., 2011; Majer et al., 2019a, 2019b).

    Article Title: The Chaperone UNC93B1 Regulates Toll-like Receptor Stability Independently of Endosomal TLR Transport.
    Article Snippet: Various studies in mouse also suggest a regulatory function of UNC93B1 in the fine-tuning of NA-sensing TLR responses (Fukui et al., 2009; Lee et al., 2013) and show that dysregulation at the level of UNC93B1 leads to autoinflammatory diseases (Fukui et al., 2011).

    Protease Inhibitor:

    Article Title: Unc93b1 is essential for cytokine activation of five PAMPs in the orange-spotted grouper (Epinephelus coioides).
    Article Snippet: 19 Toll-like receptors (TLRs) are important innate immune receptors that recognize 20 multiple pathogen-associated molecular patterns (PAMPs) and activate the immune 21 responses to resist the invasion of pathogens.. Many TLRs need assistance from 22 trafficking chaperones to transport to the specific cell compartments and then are 23 processed before they are activated.. In this study, we identified an important 24 trafficking chaperone, UNC93 homologue B1 (unc93b1), from the Epinephelus 25 coioides (orange-spotted grouper).

    Article Title: Toll-like Receptors in the Vascular System: Sensing the Dangers Within
    Article Snippet: UNC93B1 also regulates excessive TLR7 signaling by recruiting TLR9 to counteract TLR7 ( Fukui et al., 2009 ).

    Article Title: Toll-like receptor signaling in teleosts.
    Article Snippet: Toll-like receptors (TLRs) sit at the top of the immune system pyramid.. They form a paramount family of immune sentinels capable of sensing diverse microbe-associated molecular patterns (MAPMs), danger/damage-associated molecular patterns (DAMPs), and other signals.. These perceptions trigger immediate innate immunity and instruct subsequent adaptive immunity.

    Article Title: Microbial Sensing by Toll-Like Receptors and Intracellular Nucleic Acid Sensors
    Article Snippet: Further, UNC93B1 actively and continuously regulates excessive TLR7 activation of immune cells by using TLR9 to counteract TLR7 as shown by mice harboring an amino acid substitution (D34 to A) in UNC93B1, that shows TLR7-hyperreactive and TLR9-hyporeactive phenotype and subsequent TLR7-dependent systemic lethal inflammation, thereby supporting the understanding that an opposing relationship between TLR7 and TLR9 is a potential mechanism regulating autoimmunity ( Fukui et al. 2011 ).

    Article Title: Human antimicrobial peptides in ocular surface defense.
    Article Snippet: Mice deficient in UNC93B1, an essential protein that is required for TLR3, TLR7 923 and TLR9 activation, are highly susceptible to infection with T. cruzi (Caetano et al., 924 2011; Fukui et al., 2009).

    Article Title: The Chaperone UNC93B1 Regulates Toll-like Receptor Stability Independently of Endosomal TLR Transport.
    Article Snippet: Second, UNC93B1 has been shown to act as a key regulator of NA-sensing TLRs (Fukui et al., 2011; Fukui et al., 2009).

    Article Title: Gain-of-function human UNC93B1 variants cause systemic lupus erythematosus and chilblain lupus.
    Article Snippet: Mouse UNC93B1 is best known for mediating TLR signaling through the trafficking of TLR3, 7, and 9 (Kim et al., 2008; Fukui et al., 2011; Majer et al., 2019a, 2019b).

    Article Title: The Chaperone UNC93B1 Regulates Toll-like Receptor Stability Independently of Endosomal TLR Transport.
    Article Snippet: Various studies in mouse also suggest a regulatory function of UNC93B1 in the fine-tuning of NA-sensing TLR responses (Fukui et al., 2009; Lee et al., 2013) and show that dysregulation at the level of UNC93B1 leads to autoinflammatory diseases (Fukui et al., 2011).

    Stable Transfection:

    Article Title: Unc93b1 is essential for cytokine activation of five PAMPs in the orange-spotted grouper (Epinephelus coioides).
    Article Snippet: 19 Toll-like receptors (TLRs) are important innate immune receptors that recognize 20 multiple pathogen-associated molecular patterns (PAMPs) and activate the immune 21 responses to resist the invasion of pathogens.. Many TLRs need assistance from 22 trafficking chaperones to transport to the specific cell compartments and then are 23 processed before they are activated.. In this study, we identified an important 24 trafficking chaperone, UNC93 homologue B1 (unc93b1), from the Epinephelus 25 coioides (orange-spotted grouper).

    Article Title: Toll-like Receptors in the Vascular System: Sensing the Dangers Within
    Article Snippet: UNC93B1 also regulates excessive TLR7 signaling by recruiting TLR9 to counteract TLR7 ( Fukui et al., 2009 ).

    Article Title: Toll-like receptor signaling in teleosts.
    Article Snippet: Toll-like receptors (TLRs) sit at the top of the immune system pyramid.. They form a paramount family of immune sentinels capable of sensing diverse microbe-associated molecular patterns (MAPMs), danger/damage-associated molecular patterns (DAMPs), and other signals.. These perceptions trigger immediate innate immunity and instruct subsequent adaptive immunity.

    Article Title: Microbial Sensing by Toll-Like Receptors and Intracellular Nucleic Acid Sensors
    Article Snippet: Further, UNC93B1 actively and continuously regulates excessive TLR7 activation of immune cells by using TLR9 to counteract TLR7 as shown by mice harboring an amino acid substitution (D34 to A) in UNC93B1, that shows TLR7-hyperreactive and TLR9-hyporeactive phenotype and subsequent TLR7-dependent systemic lethal inflammation, thereby supporting the understanding that an opposing relationship between TLR7 and TLR9 is a potential mechanism regulating autoimmunity ( Fukui et al. 2011 ).

    Article Title: Human antimicrobial peptides in ocular surface defense.
    Article Snippet: Mice deficient in UNC93B1, an essential protein that is required for TLR3, TLR7 923 and TLR9 activation, are highly susceptible to infection with T. cruzi (Caetano et al., 924 2011; Fukui et al., 2009).

    Article Title: The Chaperone UNC93B1 Regulates Toll-like Receptor Stability Independently of Endosomal TLR Transport.
    Article Snippet: Second, UNC93B1 has been shown to act as a key regulator of NA-sensing TLRs (Fukui et al., 2011; Fukui et al., 2009).

    Article Title: Gain-of-function human UNC93B1 variants cause systemic lupus erythematosus and chilblain lupus.
    Article Snippet: Mouse UNC93B1 is best known for mediating TLR signaling through the trafficking of TLR3, 7, and 9 (Kim et al., 2008; Fukui et al., 2011; Majer et al., 2019a, 2019b).

    Article Title: The Chaperone UNC93B1 Regulates Toll-like Receptor Stability Independently of Endosomal TLR Transport.
    Article Snippet: Various studies in mouse also suggest a regulatory function of UNC93B1 in the fine-tuning of NA-sensing TLR responses (Fukui et al., 2009; Lee et al., 2013) and show that dysregulation at the level of UNC93B1 leads to autoinflammatory diseases (Fukui et al., 2011).

    Isolation:

    Article Title: Unc93b1 is essential for cytokine activation of five PAMPs in the orange-spotted grouper (Epinephelus coioides).
    Article Snippet: 19 Toll-like receptors (TLRs) are important innate immune receptors that recognize 20 multiple pathogen-associated molecular patterns (PAMPs) and activate the immune 21 responses to resist the invasion of pathogens.. Many TLRs need assistance from 22 trafficking chaperones to transport to the specific cell compartments and then are 23 processed before they are activated.. In this study, we identified an important 24 trafficking chaperone, UNC93 homologue B1 (unc93b1), from the Epinephelus 25 coioides (orange-spotted grouper).

    Article Title: Toll-like Receptors in the Vascular System: Sensing the Dangers Within
    Article Snippet: UNC93B1 also regulates excessive TLR7 signaling by recruiting TLR9 to counteract TLR7 ( Fukui et al., 2009 ).

    Article Title: Toll-like receptor signaling in teleosts.
    Article Snippet: Toll-like receptors (TLRs) sit at the top of the immune system pyramid.. They form a paramount family of immune sentinels capable of sensing diverse microbe-associated molecular patterns (MAPMs), danger/damage-associated molecular patterns (DAMPs), and other signals.. These perceptions trigger immediate innate immunity and instruct subsequent adaptive immunity.

    Article Title: Microbial Sensing by Toll-Like Receptors and Intracellular Nucleic Acid Sensors
    Article Snippet: Further, UNC93B1 actively and continuously regulates excessive TLR7 activation of immune cells by using TLR9 to counteract TLR7 as shown by mice harboring an amino acid substitution (D34 to A) in UNC93B1, that shows TLR7-hyperreactive and TLR9-hyporeactive phenotype and subsequent TLR7-dependent systemic lethal inflammation, thereby supporting the understanding that an opposing relationship between TLR7 and TLR9 is a potential mechanism regulating autoimmunity ( Fukui et al. 2011 ).

    Article Title: Human antimicrobial peptides in ocular surface defense.
    Article Snippet: Mice deficient in UNC93B1, an essential protein that is required for TLR3, TLR7 923 and TLR9 activation, are highly susceptible to infection with T. cruzi (Caetano et al., 924 2011; Fukui et al., 2009).

    Article Title: The Chaperone UNC93B1 Regulates Toll-like Receptor Stability Independently of Endosomal TLR Transport.
    Article Snippet: Second, UNC93B1 has been shown to act as a key regulator of NA-sensing TLRs (Fukui et al., 2011; Fukui et al., 2009).

    Article Title: Gain-of-function human UNC93B1 variants cause systemic lupus erythematosus and chilblain lupus.
    Article Snippet: Mouse UNC93B1 is best known for mediating TLR signaling through the trafficking of TLR3, 7, and 9 (Kim et al., 2008; Fukui et al., 2011; Majer et al., 2019a, 2019b).

    Article Title: The Chaperone UNC93B1 Regulates Toll-like Receptor Stability Independently of Endosomal TLR Transport.
    Article Snippet: Various studies in mouse also suggest a regulatory function of UNC93B1 in the fine-tuning of NA-sensing TLR responses (Fukui et al., 2009; Lee et al., 2013) and show that dysregulation at the level of UNC93B1 leads to autoinflammatory diseases (Fukui et al., 2011).

    Injection:

    Article Title: Unc93b1 is essential for cytokine activation of five PAMPs in the orange-spotted grouper (Epinephelus coioides).
    Article Snippet: 19 Toll-like receptors (TLRs) are important innate immune receptors that recognize 20 multiple pathogen-associated molecular patterns (PAMPs) and activate the immune 21 responses to resist the invasion of pathogens.. Many TLRs need assistance from 22 trafficking chaperones to transport to the specific cell compartments and then are 23 processed before they are activated.. In this study, we identified an important 24 trafficking chaperone, UNC93 homologue B1 (unc93b1), from the Epinephelus 25 coioides (orange-spotted grouper).

    Article Title: Toll-like Receptors in the Vascular System: Sensing the Dangers Within
    Article Snippet: UNC93B1 also regulates excessive TLR7 signaling by recruiting TLR9 to counteract TLR7 ( Fukui et al., 2009 ).

    Article Title: Toll-like receptor signaling in teleosts.
    Article Snippet: Toll-like receptors (TLRs) sit at the top of the immune system pyramid.. They form a paramount family of immune sentinels capable of sensing diverse microbe-associated molecular patterns (MAPMs), danger/damage-associated molecular patterns (DAMPs), and other signals.. These perceptions trigger immediate innate immunity and instruct subsequent adaptive immunity.

    Article Title: Microbial Sensing by Toll-Like Receptors and Intracellular Nucleic Acid Sensors
    Article Snippet: Further, UNC93B1 actively and continuously regulates excessive TLR7 activation of immune cells by using TLR9 to counteract TLR7 as shown by mice harboring an amino acid substitution (D34 to A) in UNC93B1, that shows TLR7-hyperreactive and TLR9-hyporeactive phenotype and subsequent TLR7-dependent systemic lethal inflammation, thereby supporting the understanding that an opposing relationship between TLR7 and TLR9 is a potential mechanism regulating autoimmunity ( Fukui et al. 2011 ).

    Article Title: Human antimicrobial peptides in ocular surface defense.
    Article Snippet: Mice deficient in UNC93B1, an essential protein that is required for TLR3, TLR7 923 and TLR9 activation, are highly susceptible to infection with T. cruzi (Caetano et al., 924 2011; Fukui et al., 2009).

    Article Title: The Chaperone UNC93B1 Regulates Toll-like Receptor Stability Independently of Endosomal TLR Transport.
    Article Snippet: Second, UNC93B1 has been shown to act as a key regulator of NA-sensing TLRs (Fukui et al., 2011; Fukui et al., 2009).

    Article Title: Gain-of-function human UNC93B1 variants cause systemic lupus erythematosus and chilblain lupus.
    Article Snippet: Mouse UNC93B1 is best known for mediating TLR signaling through the trafficking of TLR3, 7, and 9 (Kim et al., 2008; Fukui et al., 2011; Majer et al., 2019a, 2019b).

    Article Title: The Chaperone UNC93B1 Regulates Toll-like Receptor Stability Independently of Endosomal TLR Transport.
    Article Snippet: Various studies in mouse also suggest a regulatory function of UNC93B1 in the fine-tuning of NA-sensing TLR responses (Fukui et al., 2009; Lee et al., 2013) and show that dysregulation at the level of UNC93B1 leads to autoinflammatory diseases (Fukui et al., 2011).

    Concentration Assay:

    Article Title: Unc93b1 is essential for cytokine activation of five PAMPs in the orange-spotted grouper (Epinephelus coioides).
    Article Snippet: 19 Toll-like receptors (TLRs) are important innate immune receptors that recognize 20 multiple pathogen-associated molecular patterns (PAMPs) and activate the immune 21 responses to resist the invasion of pathogens.. Many TLRs need assistance from 22 trafficking chaperones to transport to the specific cell compartments and then are 23 processed before they are activated.. In this study, we identified an important 24 trafficking chaperone, UNC93 homologue B1 (unc93b1), from the Epinephelus 25 coioides (orange-spotted grouper).

    Article Title: Toll-like Receptors in the Vascular System: Sensing the Dangers Within
    Article Snippet: UNC93B1 also regulates excessive TLR7 signaling by recruiting TLR9 to counteract TLR7 ( Fukui et al., 2009 ).

    Article Title: Toll-like receptor signaling in teleosts.
    Article Snippet: Toll-like receptors (TLRs) sit at the top of the immune system pyramid.. They form a paramount family of immune sentinels capable of sensing diverse microbe-associated molecular patterns (MAPMs), danger/damage-associated molecular patterns (DAMPs), and other signals.. These perceptions trigger immediate innate immunity and instruct subsequent adaptive immunity.

    Article Title: Microbial Sensing by Toll-Like Receptors and Intracellular Nucleic Acid Sensors
    Article Snippet: Further, UNC93B1 actively and continuously regulates excessive TLR7 activation of immune cells by using TLR9 to counteract TLR7 as shown by mice harboring an amino acid substitution (D34 to A) in UNC93B1, that shows TLR7-hyperreactive and TLR9-hyporeactive phenotype and subsequent TLR7-dependent systemic lethal inflammation, thereby supporting the understanding that an opposing relationship between TLR7 and TLR9 is a potential mechanism regulating autoimmunity ( Fukui et al. 2011 ).

    Article Title: Human antimicrobial peptides in ocular surface defense.
    Article Snippet: Mice deficient in UNC93B1, an essential protein that is required for TLR3, TLR7 923 and TLR9 activation, are highly susceptible to infection with T. cruzi (Caetano et al., 924 2011; Fukui et al., 2009).

    Article Title: The Chaperone UNC93B1 Regulates Toll-like Receptor Stability Independently of Endosomal TLR Transport.
    Article Snippet: Second, UNC93B1 has been shown to act as a key regulator of NA-sensing TLRs (Fukui et al., 2011; Fukui et al., 2009).

    Article Title: Gain-of-function human UNC93B1 variants cause systemic lupus erythematosus and chilblain lupus.
    Article Snippet: Mouse UNC93B1 is best known for mediating TLR signaling through the trafficking of TLR3, 7, and 9 (Kim et al., 2008; Fukui et al., 2011; Majer et al., 2019a, 2019b).

    Article Title: The Chaperone UNC93B1 Regulates Toll-like Receptor Stability Independently of Endosomal TLR Transport.
    Article Snippet: Various studies in mouse also suggest a regulatory function of UNC93B1 in the fine-tuning of NA-sensing TLR responses (Fukui et al., 2009; Lee et al., 2013) and show that dysregulation at the level of UNC93B1 leads to autoinflammatory diseases (Fukui et al., 2011).

    Sterility:

    Article Title: Unc93b1 is essential for cytokine activation of five PAMPs in the orange-spotted grouper (Epinephelus coioides).
    Article Snippet: 19 Toll-like receptors (TLRs) are important innate immune receptors that recognize 20 multiple pathogen-associated molecular patterns (PAMPs) and activate the immune 21 responses to resist the invasion of pathogens.. Many TLRs need assistance from 22 trafficking chaperones to transport to the specific cell compartments and then are 23 processed before they are activated.. In this study, we identified an important 24 trafficking chaperone, UNC93 homologue B1 (unc93b1), from the Epinephelus 25 coioides (orange-spotted grouper).

    Article Title: Toll-like Receptors in the Vascular System: Sensing the Dangers Within
    Article Snippet: UNC93B1 also regulates excessive TLR7 signaling by recruiting TLR9 to counteract TLR7 ( Fukui et al., 2009 ).

    Article Title: Toll-like receptor signaling in teleosts.
    Article Snippet: Toll-like receptors (TLRs) sit at the top of the immune system pyramid.. They form a paramount family of immune sentinels capable of sensing diverse microbe-associated molecular patterns (MAPMs), danger/damage-associated molecular patterns (DAMPs), and other signals.. These perceptions trigger immediate innate immunity and instruct subsequent adaptive immunity.

    Article Title: Microbial Sensing by Toll-Like Receptors and Intracellular Nucleic Acid Sensors
    Article Snippet: Further, UNC93B1 actively and continuously regulates excessive TLR7 activation of immune cells by using TLR9 to counteract TLR7 as shown by mice harboring an amino acid substitution (D34 to A) in UNC93B1, that shows TLR7-hyperreactive and TLR9-hyporeactive phenotype and subsequent TLR7-dependent systemic lethal inflammation, thereby supporting the understanding that an opposing relationship between TLR7 and TLR9 is a potential mechanism regulating autoimmunity ( Fukui et al. 2011 ).

    Article Title: Human antimicrobial peptides in ocular surface defense.
    Article Snippet: Mice deficient in UNC93B1, an essential protein that is required for TLR3, TLR7 923 and TLR9 activation, are highly susceptible to infection with T. cruzi (Caetano et al., 924 2011; Fukui et al., 2009).

    Article Title: The Chaperone UNC93B1 Regulates Toll-like Receptor Stability Independently of Endosomal TLR Transport.
    Article Snippet: Second, UNC93B1 has been shown to act as a key regulator of NA-sensing TLRs (Fukui et al., 2011; Fukui et al., 2009).

    Article Title: Gain-of-function human UNC93B1 variants cause systemic lupus erythematosus and chilblain lupus.
    Article Snippet: Mouse UNC93B1 is best known for mediating TLR signaling through the trafficking of TLR3, 7, and 9 (Kim et al., 2008; Fukui et al., 2011; Majer et al., 2019a, 2019b).

    Article Title: The Chaperone UNC93B1 Regulates Toll-like Receptor Stability Independently of Endosomal TLR Transport.
    Article Snippet: Various studies in mouse also suggest a regulatory function of UNC93B1 in the fine-tuning of NA-sensing TLR responses (Fukui et al., 2009; Lee et al., 2013) and show that dysregulation at the level of UNC93B1 leads to autoinflammatory diseases (Fukui et al., 2011).

    Mouse Assay:

    Article Title: Unc93b1 is essential for cytokine activation of five PAMPs in the orange-spotted grouper (Epinephelus coioides).
    Article Snippet: 19 Toll-like receptors (TLRs) are important innate immune receptors that recognize 20 multiple pathogen-associated molecular patterns (PAMPs) and activate the immune 21 responses to resist the invasion of pathogens.. Many TLRs need assistance from 22 trafficking chaperones to transport to the specific cell compartments and then are 23 processed before they are activated.. In this study, we identified an important 24 trafficking chaperone, UNC93 homologue B1 (unc93b1), from the Epinephelus 25 coioides (orange-spotted grouper).

    Article Title: Toll-like Receptors in the Vascular System: Sensing the Dangers Within
    Article Snippet: UNC93B1 also regulates excessive TLR7 signaling by recruiting TLR9 to counteract TLR7 ( Fukui et al., 2009 ).

    Article Title: Toll-like receptor signaling in teleosts.
    Article Snippet: Toll-like receptors (TLRs) sit at the top of the immune system pyramid.. They form a paramount family of immune sentinels capable of sensing diverse microbe-associated molecular patterns (MAPMs), danger/damage-associated molecular patterns (DAMPs), and other signals.. These perceptions trigger immediate innate immunity and instruct subsequent adaptive immunity.

    Article Title: Microbial Sensing by Toll-Like Receptors and Intracellular Nucleic Acid Sensors
    Article Snippet: Further, UNC93B1 actively and continuously regulates excessive TLR7 activation of immune cells by using TLR9 to counteract TLR7 as shown by mice harboring an amino acid substitution (D34 to A) in UNC93B1, that shows TLR7-hyperreactive and TLR9-hyporeactive phenotype and subsequent TLR7-dependent systemic lethal inflammation, thereby supporting the understanding that an opposing relationship between TLR7 and TLR9 is a potential mechanism regulating autoimmunity ( Fukui et al. 2011 ).

    Article Title: Human antimicrobial peptides in ocular surface defense.
    Article Snippet: Mice deficient in UNC93B1, an essential protein that is required for TLR3, TLR7 923 and TLR9 activation, are highly susceptible to infection with T. cruzi (Caetano et al., 924 2011; Fukui et al., 2009).

    Article Title: The Chaperone UNC93B1 Regulates Toll-like Receptor Stability Independently of Endosomal TLR Transport.
    Article Snippet: Second, UNC93B1 has been shown to act as a key regulator of NA-sensing TLRs (Fukui et al., 2011; Fukui et al., 2009).

    Article Title: Gain-of-function human UNC93B1 variants cause systemic lupus erythematosus and chilblain lupus.
    Article Snippet: Mouse UNC93B1 is best known for mediating TLR signaling through the trafficking of TLR3, 7, and 9 (Kim et al., 2008; Fukui et al., 2011; Majer et al., 2019a, 2019b).

    Article Title: The Chaperone UNC93B1 Regulates Toll-like Receptor Stability Independently of Endosomal TLR Transport.
    Article Snippet: Various studies in mouse also suggest a regulatory function of UNC93B1 in the fine-tuning of NA-sensing TLR responses (Fukui et al., 2009; Lee et al., 2013) and show that dysregulation at the level of UNC93B1 leads to autoinflammatory diseases (Fukui et al., 2011).

    Activation Assay:

    Article Title: Unc93b1 is essential for cytokine activation of five PAMPs in the orange-spotted grouper (Epinephelus coioides).
    Article Snippet: 19 Toll-like receptors (TLRs) are important innate immune receptors that recognize 20 multiple pathogen-associated molecular patterns (PAMPs) and activate the immune 21 responses to resist the invasion of pathogens.. Many TLRs need assistance from 22 trafficking chaperones to transport to the specific cell compartments and then are 23 processed before they are activated.. In this study, we identified an important 24 trafficking chaperone, UNC93 homologue B1 (unc93b1), from the Epinephelus 25 coioides (orange-spotted grouper).

    Article Title: Toll-like Receptors in the Vascular System: Sensing the Dangers Within
    Article Snippet: UNC93B1 also regulates excessive TLR7 signaling by recruiting TLR9 to counteract TLR7 ( Fukui et al., 2009 ).

    Article Title: Toll-like receptor signaling in teleosts.
    Article Snippet: Toll-like receptors (TLRs) sit at the top of the immune system pyramid.. They form a paramount family of immune sentinels capable of sensing diverse microbe-associated molecular patterns (MAPMs), danger/damage-associated molecular patterns (DAMPs), and other signals.. These perceptions trigger immediate innate immunity and instruct subsequent adaptive immunity.

    Article Title: Microbial Sensing by Toll-Like Receptors and Intracellular Nucleic Acid Sensors
    Article Snippet: Further, UNC93B1 actively and continuously regulates excessive TLR7 activation of immune cells by using TLR9 to counteract TLR7 as shown by mice harboring an amino acid substitution (D34 to A) in UNC93B1, that shows TLR7-hyperreactive and TLR9-hyporeactive phenotype and subsequent TLR7-dependent systemic lethal inflammation, thereby supporting the understanding that an opposing relationship between TLR7 and TLR9 is a potential mechanism regulating autoimmunity ( Fukui et al. 2011 ).

    Article Title: Human antimicrobial peptides in ocular surface defense.
    Article Snippet: Mice deficient in UNC93B1, an essential protein that is required for TLR3, TLR7 923 and TLR9 activation, are highly susceptible to infection with T. cruzi (Caetano et al., 924 2011; Fukui et al., 2009).

    Article Title: The Chaperone UNC93B1 Regulates Toll-like Receptor Stability Independently of Endosomal TLR Transport.
    Article Snippet: Second, UNC93B1 has been shown to act as a key regulator of NA-sensing TLRs (Fukui et al., 2011; Fukui et al., 2009).

    Article Title: Gain-of-function human UNC93B1 variants cause systemic lupus erythematosus and chilblain lupus.
    Article Snippet: Mouse UNC93B1 is best known for mediating TLR signaling through the trafficking of TLR3, 7, and 9 (Kim et al., 2008; Fukui et al., 2011; Majer et al., 2019a, 2019b).

    Article Title: The Chaperone UNC93B1 Regulates Toll-like Receptor Stability Independently of Endosomal TLR Transport.
    Article Snippet: Various studies in mouse also suggest a regulatory function of UNC93B1 in the fine-tuning of NA-sensing TLR responses (Fukui et al., 2009; Lee et al., 2013) and show that dysregulation at the level of UNC93B1 leads to autoinflammatory diseases (Fukui et al., 2011).

    Infection:

    Article Title: Unc93b1 is essential for cytokine activation of five PAMPs in the orange-spotted grouper (Epinephelus coioides).
    Article Snippet: 19 Toll-like receptors (TLRs) are important innate immune receptors that recognize 20 multiple pathogen-associated molecular patterns (PAMPs) and activate the immune 21 responses to resist the invasion of pathogens.. Many TLRs need assistance from 22 trafficking chaperones to transport to the specific cell compartments and then are 23 processed before they are activated.. In this study, we identified an important 24 trafficking chaperone, UNC93 homologue B1 (unc93b1), from the Epinephelus 25 coioides (orange-spotted grouper).

    Article Title: Toll-like Receptors in the Vascular System: Sensing the Dangers Within
    Article Snippet: UNC93B1 also regulates excessive TLR7 signaling by recruiting TLR9 to counteract TLR7 ( Fukui et al., 2009 ).

    Article Title: Toll-like receptor signaling in teleosts.
    Article Snippet: Toll-like receptors (TLRs) sit at the top of the immune system pyramid.. They form a paramount family of immune sentinels capable of sensing diverse microbe-associated molecular patterns (MAPMs), danger/damage-associated molecular patterns (DAMPs), and other signals.. These perceptions trigger immediate innate immunity and instruct subsequent adaptive immunity.

    Article Title: Microbial Sensing by Toll-Like Receptors and Intracellular Nucleic Acid Sensors
    Article Snippet: Further, UNC93B1 actively and continuously regulates excessive TLR7 activation of immune cells by using TLR9 to counteract TLR7 as shown by mice harboring an amino acid substitution (D34 to A) in UNC93B1, that shows TLR7-hyperreactive and TLR9-hyporeactive phenotype and subsequent TLR7-dependent systemic lethal inflammation, thereby supporting the understanding that an opposing relationship between TLR7 and TLR9 is a potential mechanism regulating autoimmunity ( Fukui et al. 2011 ).

    Article Title: Human antimicrobial peptides in ocular surface defense.
    Article Snippet: Mice deficient in UNC93B1, an essential protein that is required for TLR3, TLR7 923 and TLR9 activation, are highly susceptible to infection with T. cruzi (Caetano et al., 924 2011; Fukui et al., 2009).

    Article Title: The Chaperone UNC93B1 Regulates Toll-like Receptor Stability Independently of Endosomal TLR Transport.
    Article Snippet: Second, UNC93B1 has been shown to act as a key regulator of NA-sensing TLRs (Fukui et al., 2011; Fukui et al., 2009).

    Article Title: Gain-of-function human UNC93B1 variants cause systemic lupus erythematosus and chilblain lupus.
    Article Snippet: Mouse UNC93B1 is best known for mediating TLR signaling through the trafficking of TLR3, 7, and 9 (Kim et al., 2008; Fukui et al., 2011; Majer et al., 2019a, 2019b).

    Article Title: The Chaperone UNC93B1 Regulates Toll-like Receptor Stability Independently of Endosomal TLR Transport.
    Article Snippet: Various studies in mouse also suggest a regulatory function of UNC93B1 in the fine-tuning of NA-sensing TLR responses (Fukui et al., 2009; Lee et al., 2013) and show that dysregulation at the level of UNC93B1 leads to autoinflammatory diseases (Fukui et al., 2011).



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    Image Search Results


    Amino acid identity comparison ( <xref ref-type= Li et al., 2015 ; Madeira et al., 2019 ) of human protein sequences of UNC93A, UNC93B1, and MFSD11 and their identified orthologs." width="100%" height="100%">

    Journal: Frontiers in Cell and Developmental Biology

    Article Title: CG4928 Is Vital for Renal Function in Fruit Flies and Membrane Potential in Cells: A First In-Depth Characterization of the Putative Solute Carrier UNC93A

    doi: 10.3389/fcell.2020.580291

    Figure Lengend Snippet: Amino acid identity comparison ( Li et al., 2015 ; Madeira et al., 2019 ) of human protein sequences of UNC93A, UNC93B1, and MFSD11 and their identified orthologs.

    Article Snippet: According to NCBI and the human protein atlas , UNC93B1 is abundantly expressed in the body, whereas UNC93A is mainly expressed in the digestive tract and the kidney ( ; ).

    Techniques: Comparison

    CG4928 is evolutionary conserved and crucial for normal renal function in D. melanogaster . Related proteins to UNC93A were searched for using a hidden Markov model. (A) UNC93A had orthologs in A. aegypti , A. carolinensis , C. elegans , C. intestinalis , D. rerio, D. melanogaster , G. aculeatus , G. gallus , and M. musculus . Closest relatives were UNC93B1 and MFSD11. CG4928 was ubiquitously knocked down using Da-Gal4 . (B) CG4928 knockdown males and females developed edema in 28°C compared with Driver control and RNAi control. Bright-field images displaying the Malpighian tubules obtained from Driver control, RNAi control, and CG4928 knockdown females were captured where (C) CG4928 knockdowns showed an accumulation of yellow-colored pigments in the Malpighian tubules, close-up (C) I–III. Ramsay assay was performed on Malpighian tubules from adult females ( n = 50). Secretion rate was measured after 2 h of secretion, average secretion rate (±SD) was plotted, and differences were calculated using one-way ANOVA with Bonferroni’s corrections (* p < 0.05, ** p < 0.01, *** p < 0.001). (D) CG4928 knockdown flies had a lower secretion rate compared with controls. Body and hemolymph samples were collected to measure osmolality, differences in body and hemolymph weight, and concentrations of sodium and potassium. Then, 20 μl of hemolymph sample from adult flies ( CG4928 knockdown n = 500, Driver control n = 800, RNAi control n = 800) was collected to measure osmolality and sodium and potassium concentrations. (E) CG4928 knockdowns had lower osmolality. Body and hemolymph weight were measured in males and females ( n = 30); weight was calculated against the number of flies. Graphs represent mean (±SD); differences were calculated with Kruskal–Wallis and Dunn’s correction (* p < 0.05, ** p > 0.01, *** p > 0.001). CG4928 knockdown flies were heavier, (F) body and (G) hemolymph weight, than controls and were found to have (H) 38.7% higher concentration of sodium and 8.6% lower concentration of potassium. Ion levels in Malpighian tubules from adult females were measured using ICP-SFMS ( n = 2–3 per genotype, with Malpighian tubules from 60 flies in each). Data are plotted with a scatter plot; differences were calculated using unpaired t -test with Bonferroni’s correction (adjusted p -values: * p < 0.0492, ** p < 0.0099, *** p < 0.0001). CG4928 knockdown flies had altered levels of (I) boron, (J) cadmium, (K) cobalt, and (L) potassium.

    Journal: Frontiers in Cell and Developmental Biology

    Article Title: CG4928 Is Vital for Renal Function in Fruit Flies and Membrane Potential in Cells: A First In-Depth Characterization of the Putative Solute Carrier UNC93A

    doi: 10.3389/fcell.2020.580291

    Figure Lengend Snippet: CG4928 is evolutionary conserved and crucial for normal renal function in D. melanogaster . Related proteins to UNC93A were searched for using a hidden Markov model. (A) UNC93A had orthologs in A. aegypti , A. carolinensis , C. elegans , C. intestinalis , D. rerio, D. melanogaster , G. aculeatus , G. gallus , and M. musculus . Closest relatives were UNC93B1 and MFSD11. CG4928 was ubiquitously knocked down using Da-Gal4 . (B) CG4928 knockdown males and females developed edema in 28°C compared with Driver control and RNAi control. Bright-field images displaying the Malpighian tubules obtained from Driver control, RNAi control, and CG4928 knockdown females were captured where (C) CG4928 knockdowns showed an accumulation of yellow-colored pigments in the Malpighian tubules, close-up (C) I–III. Ramsay assay was performed on Malpighian tubules from adult females ( n = 50). Secretion rate was measured after 2 h of secretion, average secretion rate (±SD) was plotted, and differences were calculated using one-way ANOVA with Bonferroni’s corrections (* p < 0.05, ** p < 0.01, *** p < 0.001). (D) CG4928 knockdown flies had a lower secretion rate compared with controls. Body and hemolymph samples were collected to measure osmolality, differences in body and hemolymph weight, and concentrations of sodium and potassium. Then, 20 μl of hemolymph sample from adult flies ( CG4928 knockdown n = 500, Driver control n = 800, RNAi control n = 800) was collected to measure osmolality and sodium and potassium concentrations. (E) CG4928 knockdowns had lower osmolality. Body and hemolymph weight were measured in males and females ( n = 30); weight was calculated against the number of flies. Graphs represent mean (±SD); differences were calculated with Kruskal–Wallis and Dunn’s correction (* p < 0.05, ** p > 0.01, *** p > 0.001). CG4928 knockdown flies were heavier, (F) body and (G) hemolymph weight, than controls and were found to have (H) 38.7% higher concentration of sodium and 8.6% lower concentration of potassium. Ion levels in Malpighian tubules from adult females were measured using ICP-SFMS ( n = 2–3 per genotype, with Malpighian tubules from 60 flies in each). Data are plotted with a scatter plot; differences were calculated using unpaired t -test with Bonferroni’s correction (adjusted p -values: * p < 0.0492, ** p < 0.0099, *** p < 0.0001). CG4928 knockdown flies had altered levels of (I) boron, (J) cadmium, (K) cobalt, and (L) potassium.

    Article Snippet: According to NCBI and the human protein atlas , UNC93B1 is abundantly expressed in the body, whereas UNC93A is mainly expressed in the digestive tract and the kidney ( ; ).

    Techniques: Knockdown, Control, Concentration Assay