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    Ctsd cathepsin D [ Mus musculus (house mouse) ]

    Gene ID: 13033, updated on 21-Apr-2024

    GeneRIFs: Gene References Into Functions

    GeneRIFPubMed TitleDate
    Prominent tauopathy and intracellular beta-amyloid accumulation triggered by genetic deletion of cathepsin D: implications for Alzheimer disease pathogenesis.

    Prominent tauopathy and intracellular β-amyloid accumulation triggered by genetic deletion of cathepsin D: implications for Alzheimer disease pathogenesis.
    Terron HM, Parikh SJ, Abdul-Hay SO, Sahara T, Kang D, Dickson DW, Saftig P, LaFerla FM, Lane S, Leissring MA., Free PMC Article

    04/12/2024
    Cathepsin D is the principal intracellular protease responsible for the degradation of amyloid beta-protein.

    Cathepsin D regulates cerebral Aβ42/40 ratios via differential degradation of Aβ42 and Aβ40.
    Suire CN, Abdul-Hay SO, Sahara T, Kang D, Brizuela MK, Saftig P, Dickson DW, Rosenberry TL, Leissring MA., Free PMC Article

    08/2/2022
    Lack of Cathepsin D in the central nervous system results in microglia and astrocyte activation and the accumulation of proteinopathy-related proteins.

    Lack of Cathepsin D in the central nervous system results in microglia and astrocyte activation and the accumulation of proteinopathy-related proteins.
    Suzuki C, Yamaguchi J, Sanada T, Oliva Trejo JA, Kakuta S, Shibata M, Tanida I, Uchiyama Y., Free PMC Article

    07/16/2022
    Cathepsin D interacts with adenosine A2A receptors in mouse macrophages to modulate cell surface localization and inflammatory signaling.

    Cathepsin D interacts with adenosine A(2A) receptors in mouse macrophages to modulate cell surface localization and inflammatory signaling.
    Skopál A, Kéki T, Tóth PÁ, Csóka B, Koscsó B, Németh ZH, Antonioli L, Ivessa A, Ciruela F, Virág L, Haskó G, Kókai E., Free PMC Article

    06/11/2022
    Inhibition of Extracellular Cathepsin D Reduces Hepatic Lipid Accumulation and Leads to Mild Changes in Inflammationin NASH Mice.

    Inhibition of Extracellular Cathepsin D Reduces Hepatic Lipid Accumulation and Leads to Mild Changes in Inflammationin NASH Mice.
    Yadati T, Houben T, Bitorina A, Oligschlaeger Y, Gijbels MJ, Mohren R, Lütjohann D, Khurana P, Goyal S, Kulkarni A, Theys J, Cillero-Pastor B, Shiri-Sverdlov R., Free PMC Article

    10/23/2021
    Rapid and Progressive Loss of Multiple Retinal Cell Types in Cathepsin D-Deficient Mice-An Animal Model of CLN10 Disease.

    Rapid and Progressive Loss of Multiple Retinal Cell Types in Cathepsin D-Deficient Mice-An Animal Model of CLN10 Disease.
    Bassal M, Liu J, Jankowiak W, Saftig P, Bartsch U., Free PMC Article

    10/16/2021
    Cathepsin B and D deficiency in the mouse pancreas induces impaired autophagy and chronic pancreatitis.

    Cathepsin B and D deficiency in the mouse pancreas induces impaired autophagy and chronic pancreatitis.
    Iwama H, Mehanna S, Imasaka M, Hashidume S, Nishiura H, Yamamura KI, Suzuki C, Uchiyama Y, Hatano E, Ohmuraya M., Free PMC Article

    10/16/2021
    Acid Sphingomyelinase Contributes to the Control of Mycobacterial Infection via a Signaling Cascade Leading from Reactive Oxygen Species to Cathepsin D.

    Acid Sphingomyelinase Contributes to the Control of Mycobacterial Infection via a Signaling Cascade Leading from Reactive Oxygen Species to Cathepsin D.
    Wu Y, Li C, Peng H, Swaidan A, Riehle A, Pollmeier B, Zhang Y, Gulbins E, Grassmé H., Free PMC Article

    06/19/2021
    Cathepsin D deficiency in mammary epithelium transiently stalls breast cancer by interference with mTORC1 signaling.

    Cathepsin D deficiency in mammary epithelium transiently stalls breast cancer by interference with mTORC1 signaling.
    Ketterer S, Mitschke J, Ketscher A, Schlimpert M, Reichardt W, Baeuerle N, Hess ME, Metzger P, Boerries M, Peters C, Kammerer B, Brummer T, Steinberg F, Reinheckel T., Free PMC Article

    11/21/2020
    Presynaptic Endosomal Cathepsin D Regulates the Biogenesis of GABAergic Synaptic Vesicles.

    Presynaptic Endosomal Cathepsin D Regulates the Biogenesis of GABAergic Synaptic Vesicles.
    Li X, Qin L, Li Y, Yu H, Zhang Z, Tao C, Liu Y, Xue Y, Zhang X, Xu Z, Wang Y, Lou H, Tan Z, Saftig P, Chen Z, Xu T, Bi G, Duan S, Gao Z.

    08/29/2020
    lack of cathepsin D in the renal tubular epithelial cells led to an increase of sensitivity against ischemia/reperfusion injury.

    Lack of Cathepsin D in the Renal Proximal Tubular Cells Resulted in Increased Sensitivity against Renal Ischemia/Reperfusion Injury.
    Suzuki C, Tanida I, Ohmuraya M, Oliva Trejo JA, Kakuta S, Sunabori T, Uchiyama Y., Free PMC Article

    07/27/2019
    Study shows that cathepsin D regulates lipid metabolism in murine steatohepatitis. These data demonstrate for the first time a key regulatory role for cathepsin D in lipid metabolism in the development of non-alcoholic steatohepatitis.

    Cathepsin D regulates lipid metabolism in murine steatohepatitis.
    Houben T, Oligschlaeger Y, Hendrikx T, Bitorina AV, Walenbergh SMA, van Gorp PJ, Gijbels MJJ, Friedrichs S, Plat J, Schaap FG, Lütjohann D, Hofker MH, Shiri-Sverdlov R., Free PMC Article

    01/12/2019
    Acid ceramidase inhibitor LCL521 targets lysosomes to activate cathepsin B and cathepsin D, resulting in interrupted autophagy and ER stress that culminates in myeloid-suppressor cell death.

    Ceramide activates lysosomal cathepsin B and cathepsin D to attenuate autophagy and induces ER stress to suppress myeloid-derived suppressor cells.
    Liu F, Li X, Lu C, Bai A, Bielawski J, Bielawska A, Marshall B, Schoenlein PV, Lebedyeva IO, Liu K., Free PMC Article

    02/24/2018
    Study demonstrate that PGRN interacts with the lysosomal protease CTSD and maintains its proper activity in vivo. Therefore, by regulating CTSD activity, PGRN may modulate protein homeostasis. This could potentially explain the TDP-43 aggregation observed in frontotemporal lobar degeneration with GRN mutations.

    Regulation of cathepsin D activity by the FTLD protein progranulin.
    Zhou X, Paushter DH, Feng T, Pardon CM, Mendoza CS, Hu F., Free PMC Article

    12/16/2017
    These results suggested that Purkinje cells (PCs) were more vulnerable to CTSD deficiency in lysosomes than to autophagy impairment, and this vulnerability does not depend on the severity of axonal swelling.

    Purkinje Cells Are More Vulnerable to the Specific Depletion of Cathepsin D Than to That of Atg7.
    Koike M, Shibata M, Sunabori T, Yamaguchi J, Sakimura K, Komatsu M, Tanaka K, Uchiyama Y.

    10/14/2017
    Exposure of J774A.1 cells to HOCl or HOSCN resulted in a significant decrease in the activity of the Cys-dependent cathepsins B and L, but not the Asp-dependent cathepsin D.

    Role of Myeloperoxidase Oxidants in the Modulation of Cellular Lysosomal Enzyme Function: A Contributing Factor to Macrophage Dysfunction in Atherosclerosis?
    Ismael FO, Barrett TJ, Sheipouri D, Brown BE, Davies MJ, Hawkins CL., Free PMC Article

    07/1/2017
    the cytosolic Cat D level and Cat D activity was significantly upregulated in response to oxygen-glucose deprivation/reperfusion exposure.

    Cathepsin D is involved in the oxygen and glucose deprivation/reperfusion-induced apoptosis of astrocytes.
    Liu J, Yang L, Tian H, Ma Q.

    03/11/2017
    these results suggest that inhibition of lysosomal proteases, such as CtsD, could be a new therapeutic approach to reduce renal fibrosis and slow progression of chronic kidney disease.

    Inhibition of lysosomal protease cathepsin D reduces renal fibrosis in murine chronic kidney disease.
    Fox C, Cocchiaro P, Oakley F, Howarth R, Callaghan K, Leslie J, Luli S, Wood KM, Genovese F, Sheerin NS, Moles A., Free PMC Article

    12/31/2016
    The neuroectoderm specific cathepsin D (Ctsd) knock-out mice survived about 5.5 days longer.

    Neuroectoderm-specific deletion of cathepsin D in mice models human inherited neuronal ceroid lipofuscinosis type 10.
    Ketscher A, Ketterer S, Dollwet-Mack S, Reif U, Reinheckel T.

    11/5/2016
    Data indicate that cathepsin D (CD) protein is elevated in the retinas of diabetic mice and serum of human patients with diabetic macular edema (DME).

    Cathepsin D: an Mϕ-derived factor mediating increased endothelial cell permeability with implications for alteration of the blood-retinal barrier in diabetic retinopathy.
    Monickaraj F, McGuire PG, Nitta CF, Ghosh K, Das A., Free PMC Article

    08/27/2016
    We therefore conclude that CD in pancreatic acinar cells is implicated in CB and CL degradation but not in autophagic activity.

    Cathepsin D in pancreatic acinar cells is implicated in cathepsin B and L degradation, but not in autophagic activity.
    Mehanna S, Suzuki C, Shibata M, Sunabori T, Imanaka T, Araki K, Yamamura K, Uchiyama Y, Ohmuraya M.

    05/28/2016
    This study demonistrated that Mice heterozygous for cathepsin D deficiency exhibit mania-related behavior and stress-induced depression.

    Mice heterozygous for cathepsin D deficiency exhibit mania-related behavior and stress-induced depression.
    Zhou R, Lu Y, Han Y, Li X, Lou H, Zhu L, Zhen X, Duan S.

    04/9/2016
    A proteolytic cascade, involving cathepsins C and D, controls LLOMe-mediated necrosis.

    Distinct cathepsins control necrotic cell death mediated by pyroptosis inducers and lysosome-destabilizing agents.
    Brojatsch J, Lima H Jr, Palliser D, Jacobson LS, Muehlbauer SM, Furtado R, Goldman DL, Lisanti MP, Chandran K., Free PMC Article

    01/2/2016
    Post-translational modifications drive CatD into the nucleus to cleave Histone 3 in the involuting mammary gland.

    Cleavage of Histone 3 by Cathepsin D in the involuting mammary gland.
    Khalkhali-Ellis Z, Goossens W, Margaryan NV, Hendrix MJ., Free PMC Article

    11/21/2015
    Increased lysosomal storage in CatD KO mice causes oxidative damage in brain pericytes, subsequently resulting in an increased vessel diameter and enhanced permeability of the BBB.

    Cathepsin D deficiency induces oxidative damage in brain pericytes and impairs the blood-brain barrier.
    Okada R, Wu Z, Zhu A, Ni J, Zhang J, Yoshimine Y, Peters C, Saftig P, Nakanishi H.

    10/31/2015
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