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    Litaf LPS-induced TN factor [ Mus musculus (house mouse) ]

    Gene ID: 56722, updated on 12-May-2024

    GeneRIFs: Gene References Into Functions

    GeneRIFPubMed TitleDate
    LITAF Promotes Atherosclerotic Plaque Formation by Stimulating the NF-kappaB Inflammatory Pathway.

    LITAF Promotes Atherosclerotic Plaque Formation by Stimulating the NF-κB Inflammatory Pathway.
    Li WJ, Zhou WP, Li XY, Jiang XL, Deng YC, Shen J, Xie H, Tan G, Huang L, Zhang H.

    01/4/2024
    LITAF acts as a novel regulator for pathological cardiac hypertrophy.

    LITAF acts as a novel regulator for pathological cardiac hypertrophy.
    Xiang M, Yang F, Zhou Y, Li W, Zou Y, Ye P, Zhu L, Wang PX, Chen M.

    01/15/2022
    SIMPLE Is an Endosomal Regulator That Protects Against NAFLD by Targeting the Lysosomal Degradation of EGFR.

    SIMPLE Is an Endosomal Regulator That Protects Against NAFLD by Targeting the Lysosomal Degradation of EGFR.
    Song J, Liu Y, Wan J, Zhao GN, Wang JC, Dai Z, Hu S, Yang L, Liu Z, Fu Y, Dong E, Tang YD.

    01/15/2022
    Sequential CRISPR-Based Screens Identify LITAF and CDIP1 as the Bacillus cereus Hemolysin BL Toxin Host Receptors.

    Sequential CRISPR-Based Screens Identify LITAF and CDIP1 as the Bacillus cereus Hemolysin BL Toxin Host Receptors.
    Liu J, Zuo Z, Sastalla I, Liu C, Jang JY, Sekine Y, Li Y, Pirooznia M, Leppla SH, Finkel T, Liu S., Free PMC Article

    05/29/2021
    results indicate that SIMPLE may regulate protein trafficking physiologically by localizing to the TGN and/or REs by binding PI4P.

    SIMPLE binds specifically to PI4P through SIMPLE-like domain and participates in protein trafficking in the trans-Golgi network and/or recycling endosomes.
    Moriwaki Y, Ohno Y, Ishii T, Takamura Y, Kita Y, Watabe K, Sango K, Tsuji S, Misawa H., Free PMC Article

    12/22/2018
    Suggest LITAF as regulatory of pro-inflammatory and pro-fibrogenic pattern in non-alcoholic fatty liver disease.

    LPS-induced TNF-α factor mediates pro-inflammatory and pro-fibrogenic pattern in non-alcoholic fatty liver disease.
    Ceccarelli S, Panera N, Mina M, Gnani D, De Stefanis C, Crudele A, Rychlicki C, Petrini S, Bruscalupi G, Agostinelli L, Stronati L, Cucchiara S, Musso G, Furlanello C, Svegliati-Baroni G, Nobili V, Alisi A., Free PMC Article

    10/1/2016
    Data suggest that atypical inflammatory signaling kinetics may account for the gain of function elicited by the Litaf protein SIMPLE mutation in Charcot-Marie-Tooth Type 1C (CMT1C) patients.

    Dysregulated Inflammatory Signaling upon Charcot-Marie-Tooth Type 1C Mutation of SIMPLE Protein.
    Li W, Zhu H, Zhao X, Brancho D, Liang Y, Zou Y, Bennett C, Chow CW., Free PMC Article

    09/26/2015
    Mutation of SIMPLE (Litaf) in Charcot-Marie-Tooth 1C alters production of exosomes.

    Mutation of SIMPLE in Charcot-Marie-Tooth 1C alters production of exosomes.
    Zhu H, Guariglia S, Yu RY, Li W, Brancho D, Peinado H, Lyden D, Salzer J, Bennett C, Chow CW., Free PMC Article

    12/21/2013
    This study demonistrated that loss of Litaf function is unlikely to be a major contributor to Charcot-Marie-Tooth disease, but modulating effects of macrophages need to be considered in the etiology of the disease.

    LITAF (SIMPLE) regulates Wallerian degeneration after injury but is not essential for peripheral nerve development and maintenance: implications for Charcot-Marie-Tooth disease.
    Somandin C, Gerber D, Pereira JA, Horn M, Suter U.

    01/26/2013
    Study provides evidence that LITAF contributes to the regulation of TNF-alpha in LPM harvested following acute inflammation.

    LITAF mediation of increased TNF-α secretion from inflamed colonic lamina propria macrophages.
    Bushell KN, Leeman SE, Gillespie E, Gower AC, Reed KL, Stucchi AF, Becker JM, Amar S., Free PMC Article

    03/10/2012
    In LITAF-deficient mice, mLITAF-mediated CCL2 production in macrophages was significantly reduced compared to the wild-type control animals

    Novel regulation of CCL2 gene expression by murine LITAF and STAT6B.
    Tang X, Yang Y, Amar S., Free PMC Article

    03/10/2012
    Whole-body deletion of LPS-induced TNF-alpha factor (LITAF) markedly improves experimental endotoxic shock and inflammatory arthritis.

    Whole-body deletion of LPS-induced TNF-α factor (LITAF) markedly improves experimental endotoxic shock and inflammatory arthritis.
    Merrill JC, You J, Constable C, Leeman SE, Amar S., Free PMC Article

    02/25/2012
    the regulation of LITAF/TNF-alpha by p53 and its short peptide 162-motif

    p53 peptide prevents LITAF-induced TNF-alpha-mediated mouse lung lesions and endotoxic shock.
    Tang X, O'Reilly A, Asano M, Merrill JC, Yokoyama KK, Amar S.

    01/28/2012
    PTP4A3 was identified as a novel negative regulator of LPS-induced LITAF/TNF-alpha production.

    A PTP4A3 peptide PIMAP39 modulates TNF-alpha levels and endotoxic shock.
    Tang X, Woodward T, Amar S., Free PMC Article

    08/9/2010
    LITAF is an important mediator of the LPS-induced inflammatory response.

    LPS-induced TNF-alpha factor (LITAF)-deficient mice express reduced LPS-induced cytokine: Evidence for LITAF-dependent LPS signaling pathways.
    Tang X, Metzger D, Leeman S, Amar S., Free PMC Article

    01/21/2010
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