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    SEL1L SEL1L adaptor subunit of SYVN1 ubiquitin ligase [ Homo sapiens (human) ]

    Gene ID: 6400, updated on 12-Nov-2024

    GeneRIFs: Gene References Into Functions

    GeneRIFPubMed TitleDate
    Regulation of hepatic inclusions and fibrinogen biogenesis by SEL1L-HRD1 ERAD.

    Regulation of hepatic inclusions and fibrinogen biogenesis by SEL1L-HRD1 ERAD.
    Song Z, Thepsuwan P, Hur WS, Torres M, Wu SA, Wei X, Tushi NJ, Wei J, Ferraresso F, Paton AW, Paton JC, Zheng Z, Zhang K, Fang D, Kastrup CJ, Jaiman S, Flick MJ, Sun S., Free PMC Article

    10/31/2024
    ER-associated degradation adapter Sel1L is required for CD8[+] T cell function and memory formation following acute viral infection.

    ER-associated degradation adapter Sel1L is required for CD8(+) T cell function and memory formation following acute viral infection.
    Correa-Medero LO, Jankowski SE, Hong HS, Armas ND, Vijendra AI, Reynolds MB, Fogo GM, Awad D, Dils AT, Inoki KA, Williams RG, Ye AM, Svezhova N, Gomez-Rivera F, Collins KL, O'Riordan MX, Sanderson TH, Lyssiotis CA, Carty SA., Free PMC Article

    06/14/2024
    Genome-wide screens identify SEL1L as an intracellular rheostat controlling collagen turnover.

    Genome-wide screens identify SEL1L as an intracellular rheostat controlling collagen turnover.
    Podolsky MJ, Kheyfets B, Pandey M, Beigh AH, Yang CD, Lizama CO, Datta R, Lin LL, Wang Z, Wolters PJ, McManus MT, Qi L, Atabai K., Free PMC Article

    02/23/2024
    Hypomorphic human SEL1L and HRD1 variants uncouple multilayered ER-associated degradation machinery.

    Hypomorphic human SEL1L and HRD1 variants uncouple multilayered ER-associated degradation machinery.
    Umphred-Wilson K, Adoro S., Free PMC Article

    02/6/2024
    Hypomorphic variants of SEL1L-HRD1 ER-associated degradation are associated with neurodevelopmental disorders.

    Hypomorphic variants of SEL1L-HRD1 ER-associated degradation are associated with neurodevelopmental disorders.
    Wang HH, Lin LL, Li ZJ, Wei X, Askander O, Cappuccio G, Hashem MO, Hubert L, Munnich A, Alqahtani M, Pang Q, Burmeister M, Lu Y, Poirier K, Besmond C, Sun S, Brunetti-Pierri N, Alkuraya FS, Qi L., Free PMC Article

    01/26/2024
    Association between SYVN1 and SEL1 genetic polymorphisms and remission in rheumatoid arthritis patients treated with TNF-alpha inhibitors: a machine learning approach.

    Association between SYVN1 and SEL1 genetic polymorphisms and remission in rheumatoid arthritis patients treated with TNF-α inhibitors: a machine learning approach.
    Kim W, Yeon HR, Kim JH, Kim JH, Kim JH, Kim HA, Jung JY, Kim J, Choi IA, Lee KE.

    09/25/2023
    SEL1L degradation intermediates stimulate cytosolic aggregation of polyglutamine-expanded protein.

    SEL1L degradation intermediates stimulate cytosolic aggregation of polyglutamine-expanded protein.
    Hattori T, Hanafusa K, Wada I, Hosokawa N.

    08/28/2021
    SEL1L plays a major role in human malignant gliomas.

    SEL1L plays a major role in human malignant gliomas.
    Mellai M, Annovazzi L, Boldorini R, Bertero L, Cassoni P, De Blasio P, Biunno I, Schiffer D., Free PMC Article

    06/26/2021
    Sel1L-Hrd1 ER-associated degradation maintains beta cell identity via TGF-beta signaling.

    Sel1L-Hrd1 ER-associated degradation maintains β cell identity via TGF-β signaling.
    Shrestha N, Liu T, Ji Y, Reinert RB, Torres M, Li X, Zhang M, Tang CA, Hu CA, Liu C, Naji A, Liu M, Lin JD, Kersten S, Arvan P, Qi L., Free PMC Article

    02/6/2021
    Narrowing down the Common Cytogenetic Deletion 14q to a 5.6-Mb Critical Region in 1p/19q Codeletion Oligodendroglioma-Relapsed Patients Points to Two Potential Relapse-Related Genes: SEL1L and STON2.

    Narrowing down the Common Cytogenetic Deletion 14q to a 5.6-Mb Critical Region in 1p/19q Codeletion Oligodendroglioma-Relapsed Patients Points to Two Potential Relapse-Related Genes: SEL1L and STON2.
    Zhang T, Guzman MA, Batanian JR.

    09/19/2020
    we found key statistical differences for the proteins SEL1, Notch3 and SOCS3 in the progression of uterine cervical cancer

    Protein Expression Analysis in Uterine Cervical Cancer for Potential Targets in Treatment.
    Blancas S, Medina-Berlanga R, Ortíz-García L, Loredo-Ramírez A, Santos L.

    06/15/2019
    In summary, ER retention of pathogenic VLDLR mutants involves binding to calnexin, elevated endoplasmic reticulum stress, and delayed degradation which is dependent on SEL1L.

    Degradation routes of trafficking-defective VLDLR mutants associated with Dysequilibrium syndrome.
    Kizhakkedath P, John A, Al-Gazali L, Ali BR., Free PMC Article

    12/1/2018
    Silencing of SEL1L during infection also stabilized an interaction of gO with the ER lectin OS-9, which likewise suggests that gO is an ER-associated degradation (ERAD) substrate. Taken together, our results identify an intriguing interaction of UL148 with the ERAD machinery and demonstrate that gO behaves as a constitutive ERAD substrate during infection.

    Human Cytomegalovirus Tropism Modulator UL148 Interacts with SEL1L, a Cellular Factor That Governs Endoplasmic Reticulum-Associated Degradation of the Viral Envelope Glycoprotein gO.
    Nguyen CC, Siddiquey MNA, Zhang H, Li G, Kamil JP., Free PMC Article

    09/15/2018
    Together, these results suggest that ER stress might comprise an important factor in GCD2 pathophysiology and that the effects of 4-PBA treatment might have important implications for the development of GCD2 therapeutics.

    4-Phenylbutyric acid reduces mutant-TGFBIp levels and ER stress through activation of ERAD pathway in corneal fibroblasts of granular corneal dystrophy type 2.
    Choi SI, Lee E, Jeong JB, Akuzum B, Maeng YS, Kim TI, Kim EK.

    05/27/2017
    The SEL1L critically regulates HRD1-mediated disposal of misfolded cargo through its short membrane spanning stretch.

    Association of the SEL1L protein transmembrane domain with HRD1 ubiquitin ligase regulates ERAD-L.
    Hosokawa N, Wada I.

    06/11/2016
    this is the first study reporting a significant association of the SEL1L SNP rs12435998 constitutive genetic variant with an improved overall survival in glioblastoma multiforme patients

    SEL1L SNP rs12435998, a predictor of glioblastoma survival and response to radio-chemotherapy.
    Mellai M, Cattaneo M, Storaci AM, Annovazzi L, Cassoni P, Melcarne A, De Blasio P, Schiffer D, Biunno I., Free PMC Article

    03/26/2016
    Low expression of SEL1L is associated with pancreatic ductal adenocarcinoma.

    Putative tumor suppressor gene SEL1L was downregulated by aberrantly upregulated hsa-mir-155 in human pancreatic ductal adenocarcinoma.
    Liu Q, Chen J, Wang J, Amos C, Killary AM, Sen S, Wei C, Frazier ML., Free PMC Article

    12/20/2014
    Data revealed close interaction of these two proteins in regulating the cross-talk between extracellular matrix and insulin signalling to create a favourable micro-environment for ss-cell development and function.

    SEL1L regulates adhesion, proliferation and secretion of insulin by affecting integrin signaling.
    Diaferia GR, Cirulli V, Biunno I., Free PMC Article

    08/9/2014
    SEL1L down-modulation synergy enhances valporic acid cytotoxic effects by influencing glioma stem cells proliferation and self-renewal properties.

    Down-modulation of SEL1L, an unfolded protein response and endoplasmic reticulum-associated degradation protein, sensitizes glioma stem cells to the cytotoxic effect of valproic acid.
    Cattaneo M, Baronchelli S, Schiffer D, Mellai M, Caldera V, Saccani GJ, Dalpra L, Daga A, Orlandi R, DeBlasio P, Biunno I., Free PMC Article

    04/12/2014
    ATF6 represents a novel type of ERAD-Lm substrate requiring SEL1L for degradation despite its transmembrane nature.

    The unfolded protein response transducer ATF6 represents a novel transmembrane-type endoplasmic reticulum-associated degradation substrate requiring both mannose trimming and SEL1L protein.
    Horimoto S, Ninagawa S, Okada T, Koba H, Sugimoto T, Kamiya Y, Kato K, Takeda S, Mori K., Free PMC Article

    01/4/2014
    ERdj5, by binding to Sel1L, triggers BiP-Cholera toxin interaction proximal to the Hrd1 complex; postulate this scenario enables the Hrd1-associated retrotranslocation machinery to capture the toxin efficiently once the toxin is released from BiP

    The ERdj5-Sel1L complex facilitates cholera toxin retrotranslocation.
    Williams JM, Inoue T, Banks L, Tsai B., Free PMC Article

    09/14/2013
    SEL1L expression is a potential colorectal cancer (CRC) tissue biomarker since its expression is significantly higher in adenoma cells with respect to normal mucosa; the levels of expression decrease in undifferentiated CRC cancers

    SEL1L, an UPR response protein, a potential marker of colonic cell transformation.
    Ashktorab H, Green W, Finzi G, Sessa F, Nouraie M, Lee EL, Morgano A, Moschetta A, Cattaneo M, Mariani-Costantini R, Brim H, Biunno I., Free PMC Article

    07/7/2012
    the rs12435998 SNP in SEL1L gene plays a role in modifying age at diagnosis of PDA in Caucasian nonsmokers.

    A single-nucleotide polymorphism in tumor suppressor gene SEL1L as a predictive and prognostic marker for pancreatic ductal adenocarcinoma in Caucasians.
    Liu Q, Chen J, Mai B, Amos C, Killary AM, Sen S, Wei C, Frazier ML., Free PMC Article

    06/16/2012
    Two new SEL1L variants are engaged in endosomal trafficking and secretion via vesicles, which could contribute to relieve ER stress in tumorigenic cells.

    Secretion of novel SEL1L endogenous variants is promoted by ER stress/UPR via endosomes and shed vesicles in human cancer cells.
    Cattaneo M, Lotti LV, Martino S, Alessio M, Conti A, Bachi A, Mariani-Costantini R, Biunno I., Free PMC Article

    09/3/2011
    regulation of the stability and assembly of the HRD1-SEL1L complex is critical to optimize the degradation kinetics of ERAD substrates

    SEL1L protein critically determines the stability of the HRD1-SEL1L endoplasmic reticulum-associated degradation (ERAD) complex to optimize the degradation kinetics of ERAD substrates.
    Iida Y, Fujimori T, Okawa K, Nagata K, Wada I, Hosokawa N., Free PMC Article

    07/16/2011
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