Active Cathepsin L100 ug
- Known as:
- Active Cathepsin L100 ug
- Catalog number:
- 1135-100
- Product Quantity:
- 100 ug
- Category:
- -
- Supplier:
- Biovis
- Gene target:
- Active Cathepsin L100
Related genes to: Active Cathepsin L100 ug
- Gene:
- DUSP1 NIH gene
- Name:
- dual specificity phosphatase 1
- Previous symbol:
- PTPN10
- Synonyms:
- HVH1, CL100, MKP-1
- Chromosome:
- 5q35.1
- Locus Type:
- gene with protein product
- Date approved:
- 1993-03-03
- Date modifiied:
- 2015-09-11
Related products to: Active Cathepsin L100 ug
Related articles to: Active Cathepsin L100 ug
- Diabetic kidney disease (DKD) is significantly impacting both quality of life and survival rates. The Shen-Yan-Fang-Shuai (SYFS) formula is a traditional Chinese medicine (TCM) compound widely used in the clinical treatment of DKD with proven efficacy, though its potential mechanism of action remains unclear. This study attempts to elucidate the therapeutic efficacy, mechanisms of action, and active compounds of the SYFS formula in the treatment of DKD. - Source: PubMed
Kang YiJin QianZhou MengqiZheng HuijuanLi DanwenWang XuezheZhou JingweiLv JieWang Yaoxian - , the spirochetal agent of Lyme disease, has a large array of lipoproteins that play a significant role in mediating host-pathogen interactions within ticks and vertebrates. While prior work has established that borrelial lipoproteins (LP) modulate immune signaling pathways, the broader transcriptional and proteomic programs induced by these molecules in macrophages are unclear. Here, we used integrated multi-omics approaches to characterize host signaling pathways activated specifically by purified borrelial lipoproteins in murine bone marrow derived macrophages (BMDMs). Single-cell RNA-Seq (scRNA-Seq) performed on BMDMs treated with various concentrations of borrelial lipoproteins revealed macrophage subsets within the BMDMs. Differential expression analysis showed that genes encoding various receptors, type I IFN-stimulated genes, signaling chemokines are upregulated while mitochondrial and ribosomal genes are downregulated in BMDMs in response to lipoproteins. Unbiased proteomics analysis of lysates of BMDMs treated with lipoproteins corroborated several of these findings. Notably, dual specificity phosphatase 1 () gene was upregulated during the early stages of BMDM exposure to LP. Pharmacological inhibition with benzylidene-3-cyclohexylamino-1-indanone hydrochloride (BCI), an inhibitor of both DUSP1 and 6 prior to exposure to LP, demonstrated that DUSP1 negatively regulates NLRP3-mediated pro-inflammatory signaling and positively regulates the expression of interferon-stimulated genes and those encoding , , and . Using human monocytic reporter cell lines, we showed MyD88- and IKK-dependent pathways contribute to mitochondrial alterations upon stimulation with lipoproteins. Extracellular flux analysis using the Seahorse assay revealed decreased oxygen consumption rate (OCR) and increased extracellular acidification rate (ECAR), indicating time-dependent metabolic reprogramming and a shift toward a glycolytic, pro-inflammatory metabolic state in BMDMs following LP stimulation. Collectively, these findings define signaling networks, regulatory nodes and metabolic alterations induced by borrelial lipoproteins in macrophages and highlight DUSP1 as a key modulator of lipoprotein-driven innate immune responses. This work provides a mechanistic framework for understanding how borrelial lipoproteins shape macrophage signaling, independent of the broader complexity of infection with intact pathogen. - Source: PubMed
Publication date: 2026/04/07
Kumaresan VenkateshPahari SusantaHung Chiung-YuHermann Brian PSchlesinger Larry SSeshu J - Zishen Huoxue (ZSHX) Decoction can ameliorate myocardial ischaemia by regulating the mitochondrial quality control network. However, the identification of new molecular targets is necessary for ZSHX's control of mitochondrial protein homeostasis and metabolic activities. Utilizing animal and cellular models with NDUFS4 or DUSP1, along with single-cell sequencing, metabolomics, network pharmacology, and in vivo/in vitro interventions, the study found that ischemia-reperfusion (I/R) injury triggers endoplasmic reticulum stress and mitochondrial metabolic reprogramming, accompanied by downregulation of DUSP1 and NDUFS4. Network pharmacology suggested ZSHX's role in regulating mitochondrial activity during inflammatory damage, while metabolomics confirmed that ZSHX alters metabolite composition and expression in I/R-affected tissues. Single-cell sequencing further linked I/R to disrupted mitochondrial energy metabolism and cell death, and in vitro experiments demonstrated that ZSHX preserves mitochondrial proteostasis, inhibits endoplasmic reticulum stress, restores calcium balance, upregulates DUSP1/NDUFS4 expression, and controls metabolic reprogramming to reduce myocardial inflammatory injury. Kaempferol, the primary active component of ZSHX, drives these protective effects by enhancing DUSP1/NDUFS4 expression, thereby preventing endoplasmic reticulum stress and inflammatory bursts, preserving mitochondrial function, and re-encoding mitochondrial metabolic processes post-I/R injury. - Source: PubMed
Pu XiangyiZhang QinYan ZhaoqiZhou SiyuanWu QiaominZhang XinaiCai YongyuanLiu ZhimingLiu RuxiuChang Xing - Vascular endothelial cell dysfunction leads to the breakdown of endothelial barrier integrity, which contributes to sepsis-induced acute lung injury (ALI). The study investigates the role of Cipepofol in regulating endothelial permeability and inflammation during sepsis using a cecal ligation and puncture (CLP) mouse model and human umbilical vein endothelial cells (HUVECs). Our findings demonstrate that Cipepofol treatment inhibits cytoskeletal stress fiber formation and upregulates junction proteins VE-cadherin, thereby preserving endothelial barrier function. These effects were mediated through the γ-aminobutyric acid type A (GABA) receptor α1 subunit (GABA receptor α1). Cipepofol improved sepsis outcomes, including decreased lung injury, leukocyte infiltration, and vascular permeability. Mechanistically, cipepofol-dependent GABA receptor α1 modulated the expression of dual-specificity phosphatase 1 (DUSP1) in lung tissue and endothelial cells of septic mice. DUSP1 knockdown exacerbated p38 and extracellular signal-regulated kinase (ERK)-MAPK signaling and mitochondrial dysfunction, and abolished the protective effects of Cipepofol against lipopolysaccharide (LPS)-induced mitochondrial oxidative stress. Conversely, genetic or pharmacological inhibition of GABA receptor α1 reversed Cipepofol-mediated suppression of p38/ERK-MAPK signaling and reactive oxygen species (ROS) accumulation, confirming DUSP1 as a key downstream mediator. Together, our study unveils that Cipepofol preserves endothelial integrity by depending on GABA receptor α1 to modulate DUSP1 expression, thereby suppressing p38/ERK-MAPK signaling and mitochondrial dysfunction. These findings highlight a potential therapeutic strategy for sepsis-induced ALI. Abbreviations: ALI, acute lung injury; BALF, bronchoalveolar lavage fluid; BCA, bicinchoninic acid; BSA, bovine serum albumin; CLP, cecal ligation and puncture; CIP, Cipepofol; DAPI, 4',6-diamidino-2-phenylindole; DMEM, Dulbecco's modified Eagle's medium; DUSP1, dual-specificity phosphatase 1; ECGS, endothelial cell growth supplement; ECL, enhanced chemiluminescence; ERK, extracellular signal-regulated kinase; FBS, fetal bovine serum; GABA receptor α1, γ-aminobutyric acid type A (GABA) receptor α1 subunit (GABA receptor α1); GAPDH, glyceraldehyde-3-phosphate dehydrogenase; GFP, green fluorescent protein; H&E, hematoxylin and eosin; HRP, horseradish peroxidase; HUVECs, human umbilical vein endothelial cells; ICAM-1, intercellular cell adhesion molecule-1; IL-1β, interleukin-1β; IL-6, interleukin-6; i.p., intraperitoneal; LPS, lipopolysaccharide; LV, lentiviral; MAPK, mitogen-activated protein kinase; MFI, mean fluorescence intensity; MOI, multiplicity of infection; PBS, phosphate-buffered saline; PFA, paraformaldehyde; PTX, Picrotoxin; PVDF, polyvinylidene difluoride; qRT-PCR, quantitative real-time reverse transcription polymerase chain reaction; RIPA, radioimmunoprecipitation assay; ROS, reactive oxygen species; SDS-PAGE, sodium dodecyl sulfate-polyacrylamide gel electrophoresis; SEM, standard error of the mean; shRNA, short hairpin RNA; siRNA, small interfering RNA; SOX17, SRY-box transcription factor 17; TBST, Tris-buffered saline with Tween-20; TNF-α, tumor necrosis factor-α; VCAM-1, vascular cell adhesion molecule-1; VE-cadherin, vascular endothelial cadherin; W/D, wet-to-dry; ZO-1, zonula occludens-1. - Source: PubMed
Publication date: 2026/04/19
Zhou ShutingHe XudongNi XinzheWang AizhongXu Xiaotao - Glioblastoma multiforme is an aggressive and therapy-resistant tumor, necessitating the identification of novel therapeutic targets. Here, we investigated the role of transient receptor potential vanilloid 1 (TRPV1) in mediating capsaicin-induced changes in cell viability in U87 glioblastoma cells. Wild-type cells tolerated capsaicin concentrations up to 175 μM, whereas TRPV1 knockout (TRPV1KO) cells exhibited reduced viability at 164 μM, indicating a cytoprotective function of TRPV1. Transcriptomic analyses revealed that wild-type cells activated the MAPK-MSTRG.66879-MYC-HSF1-axis, resulting in robust induction of heat shock proteins (HSPA1B, HSPA6, HSP90AA1) and dual-specificity phosphatases (DUSP1, DUSP8, DUSP10), which collectively maintained protein homeostasis and mitigated cellular damage. In contrast, TRPV1KO cells displayed impaired calcium-mediated MAPK activation, leading to altered mitochondrial oxidative phosphorylation, significant changes in electron transport chain (ETC I, II, III, IV), and enhanced intrinsic apoptosis through HRK. Notably, two long non-coding RNAs, MSTRG.56099 and MSTRG.66879, were identified as potential cis-regulators of DUSP1 and MYC, respectively. MSTRG.66879, upregulated in wild-type cells, appeared to form a TRPV1-associated regulatory axis with MYC and miR-182, promoting cell survival under capsaicin exposure. Disruption of this network in TRPV1KO cells sensitized them to capsaicin-induced apoptosis. Collectively, TRPV1 orchestrates calcium influx, MAPK signaling, heat shock protein induction, and noncoding RNA-mediated regulation to facilitate glioblastoma cell adaptation, suggesting that targeting TRPV1 and the MSTRG.66879-MYC axis may offer new therapeutic avenues and biomarkers for glioblastoma management. - Source: PubMed
Publication date: 2026/04/10
Chinreddy Subramanyam ReddyMashozhera Nicole TendayiLee GwonjinZaman IqraaPatel VaibhaviHarris Robert THankins Gerald RReddy Umesh K