| Inactivation of Cops5 in Smooth Muscle Cells Causes Abnormal Reproductive Hormone Homeostasis and Development in Mice. | Inactivation of Cops5 in Smooth Muscle Cells Causes Abnormal Reproductive Hormone Homeostasis and Development in Mice.
Huang Q, Man Y, Li W, Zhou Q, Yuan S, Yap YT, Nayak N, Zhang L, Song S, Dunbar J, Leff T, Yang X, Zhang Z., Free PMC Article | 05/15/2023 |
| JAB1 deletion in oligodendrocytes causes senescence-induced inflammation and neurodegeneration in mice. | JAB1 deletion in oligodendrocytes causes senescence-induced inflammation and neurodegeneration in mice.
Rivellini C, Porrello E, Dina G, Mrakic-Sposta S, Vezzoli A, Bacigaluppi M, Gullotta GS, Chaabane L, Leocani L, Marenna S, Colombo E, Farina C, Newcombe J, Nave KA, Pardi R, Quattrini A, Previtali SC., Free PMC Article | 04/2/2022 |
| The transcriptional cofactor Jab1/Cops5 is crucial for BMP-mediated mouse chondrocyte differentiation by repressing p53 activity. | The transcriptional cofactor Jab1/Cops5 is crucial for BMP-mediated mouse chondrocyte differentiation by repressing p53 activity.
Mamidi MK, Samsa WE, Bashur LA, Chen Y, Chan R, Lee B, Zhou G., Free PMC Article | 10/23/2021 |
| COP9 signalosome complex subunit 5, an IFT20 binding partner, is essential to maintain male germ cell survival and acrosome biogenesisdagger. | COP9 signalosome complex subunit 5, an IFT20 binding partner, is essential to maintain male germ cell survival and acrosome biogenesis†.
Huang Q, Liu H, Zeng J, Li W, Zhang S, Zhang L, Song S, Zhou T, Sutovsky M, Sutovsky P, Pardi R, Hess RA, Zhang Z., Free PMC Article | 06/12/2021 |
| Cops5 KO leads to decreased expression of the pluripotency marker Nanog, proliferation defect, G2/M cell-cycle arrest and apoptosis. | Cops5 safeguards genomic stability of embryonic stem cells through regulating cellular metabolism and DNA repair.
Li P, Gao L, Cui T, Zhang W, Zhao Z, Chen L., Free PMC Article | 06/20/2020 |
| these findings suggested that strategies based on activation of CSN5/LKB1 axis might be promising in the treatment of hypertrophic cardiomyopathy | CSN5 attenuates Ang II-induced cardiac hypertrophy through stabilizing LKB1.
Sheng Z, Xu Y, Li F, Wang S, Huang T, Lu P. | 05/23/2020 |
| Asrij sequesters CSN5 via its conserved OCIA domain, thereby preventing p53 degradation. | Asrij/OCIAD1 suppresses CSN5-mediated p53 degradation and maintains mouse hematopoietic stem cell quiescence.
Sinha S, Dwivedi TR, Yengkhom R, Bheemsetty VA, Abe T, Kiyonari H, VijayRaghavan K, Inamdar MS. | 12/28/2019 |
| Genetic deletion of Csn5 in Apoe(-/-) mice markedly exacerbated atherosclerotic lesion formation. | Inhibition of atherogenesis by the COP9 signalosome subunit 5 in vivo.
Asare Y, Ommer M, Azombo FA, Alampour-Rajabi S, Sternkopf M, Sanati M, Gijbels MJ, Schmitz C, Sinitski D, Tilstam PV, Lue H, Gessner A, Lange D, Schmid JA, Weber C, Dichgans M, Jankowski J, Pardi R, de Winther MP, Noels H, Bernhagen J., Free PMC Article | 07/14/2018 |
| CSN3 and CSN5 are involved in oocyte meiosis by regulating degradation of Cyclin B1 and Securin via APC/C. | Function of COP9 signalosome in regulation of mouse oocytes meiosis by regulating MPF activity and securing degradation.
Kim E, Yoon SJ, Kim EY, Kim Y, Lee HS, Kim KH, Lee KA., Free PMC Article | 07/20/2015 |
| COPS5 overexpression reduced spinophilin in both the cortex (19%, p < 0.05) and the hippocampus (20%, p < 0.05), leading to significant deficits in learning and memory skills | COPS5 protein overexpression increases amyloid plaque burden, decreases spinophilin-immunoreactive puncta, and exacerbates learning and memory deficits in the mouse brain.
Wang R, Wang H, Carrera I, Xu S, Lakshmana MK., Free PMC Article | 06/20/2015 |
| Jab1 is an essential regulator of early embryonic limb development. | Loss of jab1 in osteochondral progenitor cells severely impairs embryonic limb development in mice.
Bashur LA, Chen D, Chen Z, Liang B, Pardi R, Murakami S, Zhou G., Free PMC Article | 09/27/2014 |
| Lack of COPS5 in regenerating livers causes substantial replicative stress which triggers a cyclin-dependent kinase inhibitor(CDKN)2A genetic program leading to cell cycle arrest, polyploidy, and apoptosis. | The COP9 signalosome is a repressor of replicative stress responses and polyploidization in the regenerating liver.
Panattoni M, Maiorino L, Lukacs A, Zentilin L, Mazza D, Sanvito F, Sitia G, Guidotti LG, Pardi R. | 08/9/2014 |
| Jab1 may transduce laminin211 signals to regulate Schwann cell number and differentiation during axonal sorting. | Jab1 regulates Schwann cell proliferation and axonal sorting through p27.
Porrello E, Rivellini C, Dina G, Triolo D, Del Carro U, Ungaro D, Panattoni M, Feltri ML, Wrabetz L, Pardi R, Quattrini A, Previtali SC., Free PMC Article | 03/15/2014 |
| Study demonstrates that Jab1 represses chondrocyte hypertrophy in vivo, likely in part by downregulating BMP signaling and Runx2 activity. | The transcriptional co-regulator Jab1 is crucial for chondrocyte differentiation in vivo.
Chen D, Bashur LA, Liang B, Panattoni M, Tamai K, Pardi R, Zhou G., Free PMC Article | 09/14/2013 |
| Data indicate that in Cul4b-deficient embryonic fibroblasts showed Jab1 accumulation. | X-linked intellectual disability gene CUL4B targets Jab1/CSN5 for degradation and regulates bone morphogenetic protein signaling.
He F, Lu D, Jiang B, Wang Y, Liu Q, Liu Q, Shao C, Li X, Gong Y. | 07/20/2013 |
| CSN5 functions through CDK2 to control premature senescence in a novel way, depending on cyclin E in the cytoplasm. | CSN5 specifically interacts with CDK2 and controls senescence in a cytoplasmic cyclin E-mediated manner.
Yoshida A, Yoneda-Kato N, Kato JY., Free PMC Article | 06/15/2013 |
| It was shown that disruption of CSN5 prevented the formation of tumors by p53-null cells that were transformed with an active form of Ras in subcutaneously injected mice. Depletion of CSN5 suppressed cell proliferation, and induced premature senescence. | Depletion of CSN5 inhibits Ras-mediated tumorigenesis by inducing premature senescence in p53-null cells.
Tsujimoto I, Yoshida A, Yoneda-Kato N, Kato JY. | 02/23/2013 |
| These findings identify JAB1 as an important factor in checkpoint control during early B cell development, as well as in fate decisions in mature Ag-primed B cells. | JAB1 is essential for B cell development and germinal center formation and inversely regulates Fas ligand and Bcl6 expression.
Sitte S, Gläsner J, Jellusova J, Weisel F, Panattoni M, Pardi R, Gessner A. | 04/21/2012 |
| Growth factor erv1-like (Gfer) inhibits the COP9 signalosome subunit jun activation-domain binding protein 1 (Jab1)-mediated degradation of the cyclin-dependent kinase inhibitor p27(kip1) to restrict proliferation of hematopoietic stem cells. | Gfer inhibits Jab1-mediated degradation of p27kip1 to restrict proliferation of hematopoietic stem cells.
Teng EC, Todd LR, Ribar TJ, Lento W, Dimascio L, Means AR, Sankar U., Free PMC Article | 08/20/2011 |
| the COP9 signalosome subunit 5 (CSN5) is required for activation of proinflammatory kinases p38 and Erk and for down-regulation of the expression of genes regulated by nuclear factor E2-related factor 2 | Plant homologue constitutive photomorphogenesis 9 (COP9) signalosome subunit CSN5 regulates innate immune responses in macrophages.
Deng Z, Pardi R, Cheadle W, Xiang X, Zhang S, Shah SV, Grizzle W, Miller D, Mountz J, Zhang HG. | 07/9/2011 |
| Jab1 is essential for efficient DNA repair and mechanistically link Jab1 to the maintenance of genome integrity and to cell survival. | Essential roles of Jab1 in cell survival, spontaneous DNA damage and DNA repair.
Tian L, Peng G, Parant JM, Leventaki V, Drakos E, Zhang Q, Parker-Thornburg J, Shackleford TJ, Dai H, Lin SY, Lozano G, Rassidakis GZ, Claret FX., Free PMC Article | 01/15/2011 |
| CSN5/Jab1 controls different events of the cell cycle | CSN5/Jab1 controls multiple events in the mammalian cell cycle.
Yoshida A, Yoneda-Kato N, Panattoni M, Pardi R, Kato JY. | 01/1/2011 |
| the expression and function of JAB1 are critical for the proliferation and maintenance of hematopoietic progenitors | Stable form of JAB1 enhances proliferation and maintenance of hematopoietic progenitors.
Mori M, Yoneda-Kato N, Yoshida A, Kato JY., Free PMC Article | 01/21/2010 |
| Macrophage migration inhibitory factor does not modulate co-activation of androgen receptor by Jab1/CSN5. | Macrophage migration inhibitory factor does not modulate co-activation of androgen receptor by Jab1/CSN5.
Berndt K, Kim M, Meinhardt A, Klug J. | 01/21/2010 |
| Jab1 controls cell cycle progression and cell survival by regulating multiple cell cycle signaling pathways | Multiple functions of Jab1 are required for early embryonic development and growth potential in mice.
Tomoda K, Yoneda-Kato N, Fukumoto A, Yamanaka S, Kato JY. | 01/21/2010 |