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    CRELD2 cysteine rich with EGF like domains 2 [ Homo sapiens (human) ]

    Gene ID: 79174, updated on 3-Apr-2024

    GeneRIFs: Gene References Into Functions

    GeneRIFPubMed TitleDate
    CRELD2, endoplasmic reticulum stress, and human diseases.

    CRELD2, endoplasmic reticulum stress, and human diseases.
    Tang Q, Liu Q, Li Y, Mo L, He J., Free PMC Article

    03/27/2023
    Creld2 function during unfolded protein response is essential for liver metabolism homeostasis.

    Creld2 function during unfolded protein response is essential for liver metabolism homeostasis.
    Kern P, Balzer NR, Blank N, Cygon C, Wunderling K, Bender F, Frolov A, Sowa JP, Bonaguro L, Ulas T, Homrich M, Kiermaier E, Thiele C, Schultze JL, Canbay A, Bauer R, Mass E.

    10/30/2021
    ROCK-mediated selective activation of PERK signalling causes fibroblast reprogramming and tumour progression through a CRELD2-dependent mechanism.

    ROCK-mediated selective activation of PERK signalling causes fibroblast reprogramming and tumour progression through a CRELD2-dependent mechanism.
    Boyle ST, Poltavets V, Kular J, Pyne NT, Sandow JJ, Lewis AC, Murphy KJ, Kolesnikoff N, Moretti PAB, Tea MN, Tergaonkar V, Timpson P, Pitson SM, Webb AI, Whitfield RJ, Lopez AF, Kochetkova M, Samuel MS.

    10/24/2020
    intravesicular acidification by V-ATPase regulates the secretion of CRELD2 without relying on the balance of intracellular calcium ions and the expression of endoplasmic reticulum chaperones such as GRP78 and protein disulfide isomerase.

    Characterization of V-ATPase inhibitor-induced secretion of cysteine-rich with EGF-like domains 2.
    Oh-hashi K, Kanamori Y, Hirata Y, Kiuchi K.

    01/17/2015
    We demonstrate that Armet and Creld2 are genotype-specific ER stress response proteins with substrate specificities, and that aggregation of mutant matrilin-3 is a key disease trigger in MED that could be exploited as a potential therapeutic target

    Armet/Manf and Creld2 are components of a specialized ER stress response provoked by inappropriate formation of disulphide bonds: implications for genetic skeletal diseases.
    Hartley CL, Edwards S, Mullan L, Bell PA, Fresquet M, Boot-Handford RP, Briggs MD., Free PMC Article

    07/12/2014
    results strongly suggest that Creld2 may be directly regulated by BMP9 and ER stress response may play an important role in regulating osteogenic differentiation

    Endoplasmic reticulum (ER) stress inducible factor cysteine-rich with EGF-like domains 2 (Creld2) is an important mediator of BMP9-regulated osteogenic differentiation of mesenchymal stem cells.
    Zhang J, Weng Y, Liu X, Wang J, Zhang W, Kim SH, Zhang H, Li R, Kong Y, Chen X, Shui W, Wang N, Zhao C, Wu N, He Y, Nan G, Chen X, Wen S, Zhang H, Deng F, Wan L, Luu HH, Haydon RC, Shi LL, He TC, Shi Q., Free PMC Article

    05/17/2014
    Mapping of CRELD2 by FISH shows that it maps to 22q13 rather than the GenBank reported locus of 22p13.

    CRELD2: gene mapping, alternate splicing, and comparative genomic identification of the promoter region.
    Maslen CL, Babcock D, Redig JK, Kapeli K, Akkari YM, Olson SB.

    01/21/2010
    CRELD2 can act as a specific regulator of alpha4beta2 nAChR expression

    The cysteine-rich with EGF-like domains 2 (CRELD2) protein interacts with the large cytoplasmic domain of human neuronal nicotinic acetylcholine receptor alpha4 and beta2 subunits.
    Ortiz JA, Castillo M, del Toro ED, Mulet J, Gerber S, Valor LM, Sala S, Sala F, GutiƩrrez LM, Criado M.

    01/21/2010
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