| Accelerated aging in articular cartilage by ZMPSTE24 deficiency leads to osteoarthritis with impaired metabolic signaling and epigenetic regulation. | Accelerated aging in articular cartilage by ZMPSTE24 deficiency leads to osteoarthritis with impaired metabolic signaling and epigenetic regulation.
Suo J, Shao R, Yang R, Wang J, Zhang Z, Wang D, Niu N, Zheng X, Zou W., Free PMC Article | 05/31/2023 |
| Accelerated aging phenotypes in the retinal pigment epithelium of Zmpste24-deficient mice. | Accelerated aging phenotypes in the retinal pigment epithelium of Zmpste24-deficient mice.
Chae JB, Park CW, Lee HM, Choi LS, Park C, Kim J, Shin J, Hyeon J, Lee J, Lee H, Park HS, Nam CH, Chung H. | 11/5/2022 |
| The Integral Membrane Protein ZMPSTE24 Protects Cells from SARS-CoV-2 Spike-Mediated Pseudovirus Infection and Syncytia Formation. | The Integral Membrane Protein ZMPSTE24 Protects Cells from SARS-CoV-2 Spike-Mediated Pseudovirus Infection and Syncytia Formation.
Shilagardi K, Spear ED, Abraham R, Griffin DE, Michaelis S., Free PMC Article | 11/5/2022 |
| Abolishing the prelamin A ZMPSTE24 cleavage site leads to progeroid phenotypes with near-normal longevity in mice. | Abolishing the prelamin A ZMPSTE24 cleavage site leads to progeroid phenotypes with near-normal longevity in mice.
Wang Y, Shilagardi K, Hsu T, Odinammadu KO, Maruyama T, Wu W, Lin CS, Damoci CB, Spear ED, Shin JY, Hsu W, Michaelis S, Worman HJ., Free PMC Article | 03/12/2022 |
| Targeting RAS-converting enzyme 1 overcomes senescence and improves progeria-like phenotypes of ZMPSTE24 deficiency. | Targeting RAS-converting enzyme 1 overcomes senescence and improves progeria-like phenotypes of ZMPSTE24 deficiency.
Yao H, Chen X, Kashif M, Wang T, Ibrahim MX, Tüksammel E, Revêchon G, Eriksson M, Wiel C, Bergo MO., Free PMC Article | 08/28/2021 |
| Deficiency in ZMPSTE24 and resulting farnesyl-prelamin A accumulation only modestly affect mouse adipose tissue stores. | Deficiency in ZMPSTE24 and resulting farnesyl-prelamin A accumulation only modestly affect mouse adipose tissue stores.
Heizer PJ, Yang Y, Tu Y, Kim PH, Chen NY, Hu Y, Yoshinaga Y, de Jong PJ, Vergnes L, Morales JE, Li RL, Jackson N, Reue K, Young SG, Fong LG., Free PMC Article | 06/5/2021 |
| Loss of lamin A in Lmna-knockout mouse embryonic fibroblasts (MEFs) confers increased CK2 activity. Conversely, prelamin A that accumulates in Zmpste24-deficent MEFs exhibits a high CK2alpha binding affinity and concomitantly reduces CK2 kinase activity | Lamin A buffers CK2 kinase activity to modulate aging in a progeria mouse model.
Ao Y, Zhang J, Liu Z, Qian M, Li Y, Wu Z, Sun P, Wu J, Bei W, Wen J, Wu X, Li F, Zhou Z, Zhu WG, Liu B, Wang Z., Free PMC Article | 05/2/2020 |
| These results indicate that the absence of Zmpste24 in aging mice results in impaired lung fibrotic response after injury, which is likely associated to the dysregulation of fibrosis-related miRNAs. | Accelerated aging induced by deficiency of Zmpste24 protects old mice to develop bleomycin-induced pulmonary fibrosis.
Calyeca J, Balderas-Martínez YI, Olmos R, Jasso R, Maldonado V, Rivera Q, Selman M, Pardo A., Free PMC Article | 12/21/2019 |
| these findings suggest that downregulated miR3425p is involved in regulating cell proliferation and cell cycles in Zmpste24/ MEFs by suppressing GAS2 in vitro. | miR‑342‑5p promotes Zmpste24‑deficient mouse embryonic fibroblasts proliferation by suppressing GAS2.
Zhang CL, Liu X, He QJ, Zheng H, Xu S, Xiong XD, Yuan Y, Ruan J, Li JB, Xing Y, Zhou Z, Deng S., Free PMC Article | 06/30/2018 |
| ZMPSTE24 is a downstream effector of IFITM3 and is important for interferon-induced transmembrane antiviral activity. | ZMPSTE24 Is Downstream Effector of Interferon-Induced Transmembrane Antiviral Activity.
Li S, Fu B, Wang L, Dorf ME., Free PMC Article | 09/23/2017 |
| ZMPSTE24 is an important element for innate host defense against a broad spectrum of pathogenic viruses. | ZMPSTE24 defends against influenza and other pathogenic viruses.
Fu B, Wang L, Li S, Dorf ME., Free PMC Article | 08/19/2017 |
| we identified the abnormal lamin A (prelamin A), accompanied by a down-regulation of a lamin A processing enzyme (Zmpste24) in the kidney of the GMF transgenic mice | Transgenic mice overexpressing glia maturation factor-β, an oxidative stress inducible gene, show premature aging due to Zmpste24 down-regulation.
Imai R, Asai K, Hanai J, Takenaka M., Free PMC Article | 05/21/2016 |
| In Zmpste24(-/-) mice, histone H4 was hypoacetylated at a lysine 16 residue (H4K16), and this defect was attributed to the reduced association of a histone acetyltransferase, Mof, to the nuclear matrix. | Histone H4 lysine 16 hypoacetylation is associated with defective DNA repair and premature senescence in Zmpste24-deficient mice.
Krishnan V, Chow MZ, Wang Z, Zhang L, Liu B, Liu X, Zhou Z., Free PMC Article | 10/8/2011 |
| Nuclear envelope alterations generate an aging-like epigenetic pattern in mice deficient in Zmpste24 metalloprotease | Nuclear envelope alterations generate an aging-like epigenetic pattern in mice deficient in Zmpste24 metalloprotease.
Osorio FG, Varela I, Lara E, Puente XS, Espada J, Santoro R, Freije JM, Fraga MF, López-Otín C. | 03/12/2011 |
| Zmpste24-null mice show accelerated aging and exhibit an extensive basal activation of autophagy. | Premature aging in mice activates a systemic metabolic response involving autophagy induction.
Mariño G, Ugalde AP, Salvador-Montoliu N, Varela I, Quirós PM, Cadiñanos J, van der Pluijm I, Freije JM, López-Otín C. | 01/21/2010 |
| darunavir does not inhibit the biochemical activity of ZMPSTE24, nor does it lead to an accumulation of farnesyl-prelamin A in cells. | A potent HIV protease inhibitor, darunavir, does not inhibit ZMPSTE24 or lead to an accumulation of farnesyl-prelamin A in cells.
Coffinier C, Hudon SE, Lee R, Farber EA, Nobumori C, Miner JH, Andres DA, Spielmann HP, Hrycyna CA, Fong LG, Young SG., Free PMC Article | 01/21/2010 |
| Zmpste24 has a role in processing of prelamin A and lack of Zmpste24 results in a brittle bone phenotype | Zmpste24 deficiency in mice causes spontaneous bone fractures, muscle weakness, and a prelamin A processing defect.
Bergo MO, Gavino B, Ross J, Schmidt WK, Hong C, Kendall LV, Mohr A, Meta M, Genant H, Jiang Y, Wisner ER, Van Bruggen N, Carano RA, Michaelis S, Griffey SM, Young SG., Free PMC Article | 01/21/2010 |
| Zmpste24 deficiency elicits a stress signalling pathway that is evidenced by a marked upregulation of p53 target genes, and accompanied by a senescence phenotype at the cellular level and accelerated ageing at the organismal level | Accelerated ageing in mice deficient in Zmpste24 protease is linked to p53 signalling activation.
Varela I, Cadiñanos J, Pendás AM, Gutiérrez-Fernández A, Folgueras AR, Sánchez LM, Zhou Z, Rodríguez FJ, Stewart CL, Vega JA, Tryggvason K, Freije JM, López-Otín C. | 01/21/2010 |
| the progeria-like phenotypes caused by the lack of Zmpste24 in knockout mice is eliminated by heterozygosity for Lmna | Heterozygosity for Lmna deficiency eliminates the progeria-like phenotypes in Zmpste24-deficient mice.
Fong LG, Ng JK, Meta M, Coté N, Yang SH, Stewart CL, Sullivan T, Burghardt A, Majumdar S, Reue K, Bergo MO, Young SG., Free PMC Article | 01/21/2010 |
| Lack of functional Zmpste24, a metalloproteinase responsible for the maturation of prelamin A, also results in progeroid phenotypes in mice | Genomic instability in laminopathy-based premature aging.
Liu B, Wang J, Chan KM, Tjia WM, Deng W, Guan X, Huang JD, Li KM, Chau PY, Chen DJ, Pei D, Pendas AM, Cadiñanos J, López-Otín C, Tse HF, Hutchison C, Chen J, Cao Y, Cheah KS, Tryggvason K, Zhou Z. | 01/21/2010 |
| Defective prelamin A processing and muscular and adipocyte alterations in Zmpste24 metalloproteinase-deficient mice. | Defective prelamin A processing and muscular and adipocyte alterations in Zmpste24 metalloproteinase-deficient mice.
Pendás AM, Zhou Z, Cadiñanos J, Freije JM, Wang J, Hultenby K, Astudillo A, Wernerson A, Rodríguez F, Tryggvason K, López-Otín C. | 01/21/2010 |