LECT1 Blocking Peptide
- Known as:
- LECT1 Blocking Peptide
- Catalog number:
- 33r-1259
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- LECT1 Blocking Peptide
Related genes to: LECT1 Blocking Peptide
- Gene:
- CNMD NIH gene
- Name:
- chondromodulin
- Previous symbol:
- MYETS1, LECT1
- Synonyms:
- CHM-I, CHM1, BRICD3
- Chromosome:
- 13q14.3
- Locus Type:
- gene with protein product
- Date approved:
- 2003-02-18
- Date modifiied:
- 2016-10-20
Related products to: LECT1 Blocking Peptide
Related articles to: LECT1 Blocking Peptide
- Developmental dysplasia of the hip (DDH) is a common pediatric orthopedic disorder that predisposes affected children to early-onset osteoarthritis (OA), yet the cellular heterogeneity and fibrotic remodeling of acetabular cartilage are poorly understood. - Source: PubMed
Publication date: 2026/04/28
Nijiati YaxierSong JunHuang PengLin ZichenPei YingzhiNing Bo - Muscle stem cells (MuSCs) are essential for skeletal muscle regeneration and maintenance of tissue homeostasis. However, their regenerative capacity declines with aging and in several pathological conditions, including neuromuscular diseases, cancer cachexia, sepsis, and metabolic disorders. Increasing evidence has identified mitochondria as key regulators of MuSC behavior, influencing quiescence, activation, self-renewal, and differentiation during myogenesis. In addition to their role in energy production, mitochondria function as metabolic and signaling hubs that integrate cellular and environmental cues to control stem cell fate decisions. This review summarizes current knowledge on the role of mitochondria in MuSC biology, including the contribution of mitochondrial bioenergetics and metabolic signaling to MuSC state transitions, the importance of mitochondrial network dynamics in regulating stem cell function, and the role of mitochondrial quality control mechanisms such as mitophagy and selective mitochondrial inheritance. We further discuss how mitochondrial dysfunction contributes to impaired MuSC function in aging and muscle-wasting conditions and highlight potential therapeutic strategies targeting mitochondrial pathways to improve muscle regeneration. - Source: PubMed
Publication date: 2026/03/04
Khacho MireilleBurelle Yan - In Germany, patients with chronic non-malignant diseases (CNMD) are predominantly treated by general practitioners (GPs). Yet, little is known about communication between GPs and specialist palliative home care (SPHC) teams in terms of care needs and care planning for patients. Our analysis therefore aims at GPs´, SPHC nurses’ and SPHC physician’s interaction during case conferences (CCs) on patients with CNMD following an initial comprehensive palliative care consultation. - Source: PubMed
Publication date: 2026/02/26
Weber Jan PhilipMüller ChristianePohontsch Nadine JanisBöttcher SilkeSekanina UtaSchade FranziskaHummers EvaScherer MartinMarx GabriellaStiel Stephanie - Patients with progressive chronic non-malignant diseases (CNMD) such as chronic obstructive pulmonary disease, congestive heart failure and dementia could benefit from specialist palliative home care (SPHC). The two-arm, cluster randomised controlled KOPAL trial was conducted to test the effectiveness of a timely SPHC nurse-patient consultation followed by an interprofessional telephone case conference between general practitioners and SPHC teams. This study was a component of the KOPAL trial and aims to explore general practitioners' (GP) experiences with treating CNMD patients before and with case conferences and with the following consequences for treatment and interprofessional collaboration with SPHC teams. - Source: PubMed
Publication date: 2025/08/25
Marx GabriellaSchwabe SvenKuba SarahWeber Jan PhilipPohontsch Nadine JanisSchade FranziskaScherer MartinSchneider Nils - Idiopathic childhood nephrotic syndrome is a common glomerulopathy comprising proteinuria, hypoalbuminemia, and edema. Podocyte dysfunction is central to this disease process. Extracellular vesicles are released from stressed cells and can represent a molecular snapshot of the parent cell of origin. We previously showed that urinary large extracellular vesicles (LEVs) derived from podocytes are increased in patients with nephrotic syndrome relapse. Here, we investigated the role of mitochondrial DNA (mtDNA) within LEVs both in vitro and in vivo, revealing the novel finding that podocytes release LEVs containing mtDNA, driven by mitochondrial stress. A puromycin aminonucleoside nephrosis rat model showed foot process effacement on electron microscopy and urinary LEVs with significantly increased mtDNA. Prednisolone, which drives remission in nephrotic syndrome in children, attenuated mitochondrial stress and reduced the amount of mtDNA content within LEVs in vitro. Lastly, urinary LEVs from children with nephrotic syndrome also contain mtDNA, and it is the podocyte LEV-fraction which is preferentially enriched. Overall, these data support a potential mechanism of podocyte mitochondrial stress in non-genetic, idiopathic pediatric nephrotic syndrome. - Source: PubMed
Publication date: 2025/07/26
Myette Robert LHolterman Chet ETrentin-Sonoda MayraCooper Tyler TLajoie Gilles ACairns GeorgeBurelle YanEl Khatib NourRaman-Nair JoannaBurger DylanKennedy Christopher R J