Human PCSK1 Protein
- Known as:
- Human PCSK1 Protein
- Catalog number:
- PC1-H5229
- Product Quantity:
- 500ug
- Category:
- -
- Supplier:
- acrobyosystems
- Gene target:
- Human PCSK1 Protein
Related genes to: Human PCSK1 Protein
- Gene:
- PCSK1 NIH gene
- Name:
- proprotein convertase subtilisin/kexin type 1
- Previous symbol:
- NEC1
- Synonyms:
- PC1, PC3, SPC3
- Chromosome:
- 5q15
- Locus Type:
- gene with protein product
- Date approved:
- 1991-06-07
- Date modifiied:
- 2018-03-06
Related products to: Human PCSK1 Protein
Related articles to: Human PCSK1 Protein
- Corticotroph tumors (CTs) derive from the lineage and are functioning (FCTs) or nonfunctioning (NFCTs). In FCTs, the main pathogenic variants are found in enhancing proopiomelanocortin () transcription through epidermal growth factor receptor (EGFR) signaling, resulting in a higher secretion index compared with wild type (WT). POMC is cleaved by prohormone convertase 1/3, encoded by proprotein convertase subtilisin/kexin type 1 gene (), into ACTH. is inhibited by which in turn is inhibited by transcription factor paired box 6 (). We aimed to compare gene expressions involved in POMC processing among NFCTs, + FCTs, and WT FCTs. - Source: PubMed
Publication date: 2026/04/21
Lamback ElisaMiranda Renan LMendonça Laryssade Figueiredo Camila SSalum Kaio C RDezonne Rômulo SWildemberg Luiz EduardoGadelha Mônica R - Estrogen deficiency is an established risk factor for menopausal brain dysfunctions in women. Urgent exploration of drugs is needed to improve estrogen deficiency-related brain dysfunctions without the side effects of estrogen supplements. Three-month-old rats had bilateral ovariectomy (OVX) performed and were treated with emodin (EMO, 80 mg/kg/day) and 17 β-estradiol (EST, 0.5 mg/kg/day). Brain functions were evaluated by cognition and emotion-related behavioral tests. Levels of glucagon-like peptide-1 (GLP-1) and estrogen in blood, mRNA levels of estrogen receptor (ER) α, ERβ, GLP-1 receptor (GLP-1R), proprotein convertase subtilisin/kexin type 1 (PCSK1) and proglucagon (proGCG) in intestinal segments, and brain ERα and GLP-1R levels were evaluated. Contractions of isolated intestinal segments were recorded. Additionally, an ERβ antagonist, PHTPP (200 μg/kg/day), was used to clarify the role of ERβ. EST and EMO significantly ameliorated cognition deficit and depressive behaviors in OVX rats, and reduced neuronal loss and synaptic abnormalities in the hippocampus and prefrontal cortex. The blood GLP-1 levels of sham operation rats (sham, 3.09 pg/mL), EMO-treated (2.57 pg/mL) and EST-treated OVX rats (2.64 pg/mL), were higher than that of OVX rats (1.03 pg/mL). EMO had no effect on the blood estrogen level. Furthermore, EMO up-regulated mRNA levels of ERβ in ileum, colon, and cerebral GLP-1R level, while EST increased mRNA levels of ERβ in colon and cerebral ERα level. In vitro intestinal segment spontaneous contraction tests revealed that EMO reduced contraction amplitudes in isolated intestinal segments from OVX rats, with the ileum and proximal colon showing greater sensitivity to EMO. The ileum and colon segments from OVX rats were less sensitive to EST as compared to those of normal rats. Upon PHTPP intervention, the up-regulated intestinal mRNA levels of ERβ, PCSK1, proGCG, blood GLP-1 level by EMO, and the beneficial effects of EMO in abnormal behaviors of OVX rats were significantly inhibited. Overall, it was found that EMO up-regulated blood GLP-1 level via intestinal Erβ-dependent mechanism and increased brain GLP-1R level, which may be involved in the neuroprotection of EMO in OVX animals. - Source: PubMed
Publication date: 2026/04/10
Liu Xin-YuanYe Chao-YuanLiu Yuan-ChengZhao Meng-YingLi Ya-NanLin LiDu Yan-JunFang Ying-YanTian Qing - Setmelanotide, a melanocortin 4 receptor (MC4R) agonist, is a promising pharmacological treatment option for people with rare monogenic obesity conditions affecting the leptin-melanocortin signaling pathway, including proprotein convertase subtilisin/kexin type 1 (PCSK1) gene mutations. It has been studied in people with homozygous mutations causing a complete deficiency of PCSK1. We report the first case of a 40-year-old female with a heterozygous PCSK1 N221D (c.661 A>G) variant mutation leading to severe early-onset treatment-resistant obesity with previous suboptimal response to bariatric surgery and conventional obesity medications, who achieved a total weight loss of 11.8% with setmelanotide treatment over the course of 3 months. Although her mutation confers a loss of 10% to 30% enzymatic function in in vitro studies, setmelanotide was highly effective in treating her obesity. It is also the first reported case of a cutaneous adverse effect of setmelanotide in the form of severe skin hyperpigmentation in a patient with a pathogenic PCSK1 variant. This case underscores the effectiveness and safety of setmelanotide in a heterozygous PCSK1 mutation. - Source: PubMed
Publication date: 2026/05/01
Lytvyak EllinaRattol ArshdeepGrunvald Eduardo - Genes play a pivotal role in appetite regulation and energy homeostasis during a person's obesity. LEP (Leptin) and POMC (Proopiomelanocortin) are vital for appetite suppression and promoting satiety, while AgRP (Agouti-related peptide) and NPY (Neuropeptide Y) serve to stimulate appetite, creating a balanced interplay between hunger and satiety signals. GHRL (Ghrelin) further promotes hunger, emphasizing the complexity of these regulatory mechanisms. BDNF (Brain-derived neurotrophic factor) shows a dual role, impacting energy homeostasis not only in the brain but also in adipose tissue, thereby influencing lipid metabolism. PCSK1 (Proprotein Convertase Subtilisin/Kexin Type 1) is critical for the processing of neuropeptides that modulate energy balance. IGF2BP2 (Insulin-like Growth Factor 2 mRNA-Binding Protein 2) and MAP2K5 (Mitogen-Activated Protein Kinase 5) contribute to metabolic processes involved in fat accumulation and glucose regulation. Thus, emphasizing the significance of these mechanisms offers valuable insights that could lead to effective interventions for obesity prevention and management. - Source: PubMed
Kaur HarmandeepKaushik DeepikaRasane PrasadOz FatihProestos CharalamposKumar Mukul - Epigenome-wide studies of pancreatic islets provide valuable insights into type 2 diabetes (T2D) but lack methylomes from individual cell types. Here we show changes to alpha and beta cell-specific methylomes and transcriptomes from people with or without T2D, using whole-genome bisulfite sequencing and RNA sequencing. We discover 22,544 differentially methylated regions annotated to 7,975 genes in alpha versus beta cells, such as INS, GCG, PDX1 and PCSK1, with ~50% showing differential expression. CRISPR-dCas9-DNMT3A-based epigenetic editing increases INS and TH DNA methylation, while CRISPR-dCas9-TET1-based editing decreases GCG methylation, each altering INS, TH or GCG expression and content in beta cells. Pre-T2D/T2D-associated differentially methylated regions in alpha and beta cells overlap 12-18% of T2D-associated genome-wide association study candidates. Additionally, ONECUT2 is epigenetically upregulated in beta cells from people with pre-T2D/T2D and elevated in male Goto-Kakizaki rat islets. ONECUT2 overexpression in beta cells/islets downregulates gene sets impacting insulin secretion and glucose homeostasis, and reduces mitochondrial activity, ATP/ADP ratio and insulin secretion. We also provide 'alpha-beta-methylome' ( https://alpha-beta-methylome.serve.scilifelab.se/app/alpha-beta-methylome/ ), a resource exploring T2D, age and sex associations on methylation, highlighting cell-specific epigenetic regulation and dysfunctions contributing to T2D. - Source: PubMed
Publication date: 2026/04/24
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