CTSD Mouse Monoclonal Antibody
- Known as:
- CTSD Mouse Monoclonal Antibody
- Catalog number:
- BIN-001509-M01
- Product Quantity:
- 0.1mg
- Category:
- -
- Supplier:
- Zyagen
- Gene target:
- CTSD Mouse Monoclonal Antibody
Related genes to: CTSD Mouse Monoclonal Antibody
- Gene:
- CTSD NIH gene
- Name:
- cathepsin D
- Previous symbol:
- CPSD
- Synonyms:
- CLN10
- Chromosome:
- 11p15.5
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2014-11-18
Related products to: CTSD Mouse Monoclonal Antibody
Related articles to: CTSD Mouse Monoclonal Antibody
- Cathepsins play critical roles in various physiopathological processes, with several reported to be associated with nonalcoholic fatty liver disease (NAFLD). Herein, we investigated the expression patterns of the cathepsin family in human and mouse livers, cultured hepatocytes, and their roles in NAFLD. Public datasets of NAFLD patients and controls were analyzed to examine hepatic cathepsin expression in human livers. RT-qPCR assessed these genes in mouse livers, HepG2, Hepa1-6, and mouse primary cells. Despite different expression patterns, CTSA, CTSB, CTSD, CTSH, and CTSL were consistently highly expressed across all samples. Notably, steatosis patients and diabetic mice exhibited significantly increased hepatic expression of four cathepsins. Among these, we first observed elevated CTSG and CTSW, with CTSG showing the most pronounced increase. Moreover, hepatic CTSG was increased and positively correlated with disease severity in NASH patients. CTSG was also upregulated in HepG2 cells treated with high glucose or free fatty acids. In vitro, CTSG overexpression promoted, while its knockdown reduced lipid accumulation. In vivo, hepatic CTSG overexpression significantly induced lipid deposition, impaired glucose tolerance, and elevated HOMA-IR. Mechanistically, CTSG upregulated key lipid synthesis genes (ACC, SCD1) and downregulated those involved in lipid oxidation (PPARα, Lcad) and secretion (MTTP) by suppressing Akt. Furthermore, Akt activation alleviated lipid deposition induced by CTSG overexpression, while Akt inhibition abolished the beneficial effect of CTSG knockdown. This study is the first to reveal the expression patterns of the cathepsin family in human and mouse livers, and identifies that hepatic CTSG is elevated in NAFLD and can promote lipid deposition, supporting CTSG as a novel potential therapeutic target for NAFLD. - Source: PubMed
Yang WeiliLin JiaqiPan QiuyueJiang YanShi TingtingCao Xi - TFEB acts as a master transcriptional regulator of lysosomal activity, which is central to host antiviral defense. Multiple viruses target TFEB to evade lysosomal degradation in host cells. This study investigated how HBV suppresses TFEB via NSUN2-mediated mC RNA modification. - Source: PubMed
Publication date: 2026/04/11
Dong XuejiaoDing ShuangHe LiliLuo FuyuCui ZhangboTang ShiZhan GuanliHao HaojieGuan WuxiangShi Chunwei - Autopsy of two adults with lifelong severe intellectual disability revealed four-repeat tauopathy. One case showed typical progressive supranuclear palsy, whereas the other demonstrated a PSP-like phenotype with restricted basal ganglia-brainstem involvement. Molecular autopsy identified variants in SPG7 and CTSD, suggesting intracellular vulnerability. These findings expand the neuropathological spectrum of severe intellectual disability and indicate that primary four-repeat tauopathy may occur in this underrecognised population. - Source: PubMed
Hata YukikoKaneko HiroyaYoshida KojiTanaka RyoIchimata ShojiroNishida Naoki - Acute kidney injury (AKI) is characterized by a rapid decline in renal function and is associated with high mortality worldwide. Transcription factor EB (TFEB), a master regulator of lysosomal biogenesis, exerts protective effects in AKI, although the underlying mechanisms remain unclear. Exosomes derived from multivesicular bodies (MVBs) play diverse roles in kidney diseases. Emerging evidence suggests that lysosome-dependent degradation of MVBs plays an important role in regulating exosome secretion. Based on this, TFEB may inhibit exosome secretion by promoting lysosomal biogenesis and lysosome-dependent degradation of MVBs, thereby attenuating AKI progression. - Source: PubMed
Publication date: 2026/04/06
Xu ZhifengXiang HuilingLiu HuixiaZhang ChunZhang XiaoliXiong Jing - Apolipoprotein B (APOB), a structural component of low-density lipoproteins (LDL), has historically been associated with peripheral lipid transport and cardiovascular disease. Recent studies have revealed a link between APOB and Alzheimer's disease (AD), with increased cerebrospinal fluid (CSF) APOB levels correlating with tau pathology. Although APOB is known to be locally expressed in the brain, albeit at very low levels, its function in the central nervous system and contribution to neurodegenerative processes remains poorly understood. To investigate the effects of chronic APOB overexpression on brain molecular homeostasis, we used a transgenic mouse model expressing human APOB-100 and integrated findings with human cohort data to assess its functional relevance to AD pathology. - Source: PubMed
Publication date: 2026/04/02
Aumont-Rodrigue GabrielPoirier AlexandrePicard CynthiaPoirier Judes