Human Kininogen 1 / KNG1 (LMW) Protein
- Known as:
- Human Kininogen 1 / KNG1 (LMW) Protein
- Catalog number:
- KN1-H5225
- Product Quantity:
- 1mg
- Category:
- -
- Supplier:
- acrobyosystems
- Gene target:
- Human Kininogen 1 / KNG1 (LMW) Protein
Related genes to: Human Kininogen 1 / KNG1 (LMW) Protein
- Gene:
- ACP1 NIH gene
- Name:
- acid phosphatase 1
- Previous symbol:
- -
- Synonyms:
- HAAP, LMW-PTP, LMWPTP
- Chromosome:
- 2p25.3
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2017-09-15
- Gene:
- KNG1 NIH gene
- Name:
- kininogen 1
- Previous symbol:
- KNG, BDK
- Synonyms:
- BK
- Chromosome:
- 3q27.3
- Locus Type:
- gene with protein product
- Date approved:
- 1990-07-26
- Date modifiied:
- 2019-04-23
Related products to: Human Kininogen 1 / KNG1 (LMW) Protein
Related articles to: Human Kininogen 1 / KNG1 (LMW) Protein
- Fasting triggers profound systemic metabolic adaptations that are essential for survival during nutrient scarcity, yet the temporal dynamics and cross-tissue coordination of proteomic remodeling remain incompletely characterized. Here, we employed quantitative proteomics to systematically profile the gastrocnemius (GA) muscle and liver of mice subjected to a 72 h fasting challenge at five time points (0, 12, 24, 48, and 72 h). Principal component analysis and hierarchical clustering revealed progressive, time-dependent proteomic reprogramming in both tissues, with distinct temporal trajectories of differentially expressed proteins (DEPs). GA muscle exhibited a biphasic response, with maximal downregulation at 48 h and peak upregulation at 72 h, whereas liver displayed a monotonic increase in DEPs, predominantly characterized by suppression of anabolic programs. Integrative cross-tissue analysis identified 97 conserved fasting-responsive proteins, including molecular chaperones (HSPA5, HSP90B1), complement components (C3), and coagulation factors (FGA, KNG1), which formed highly interconnected protein-protein interaction hubs. Fuzzy c-means clustering resolved five major temporal expression modules in each tissue, revealing coordinated shifts in mitochondrial metabolism, proteostasis, translation, and stress-response pathways. Spearman correlation analysis demonstrated moderate yet stable cross-tissue concordance (r = 0.43-0.48) throughout fasting, suggesting shared systemic regulatory mechanisms. Collectively, our findings provide a comprehensive temporal atlas of fasting-induced proteomic remodeling, revealing tissue-specific adaptive strategies alongside conserved molecular programs that orchestrate multi-organ metabolic homeostasis during prolonged nutrient deprivation. - Source: PubMed
Publication date: 2026/05/21
Cui LeileiZeng LinYang MengqiWang QiquanHuang ChunpingLin LiangLi PingLiu TaoTong WeipengSun JiayiWei HuiLan XinqiangXiang YangSu YuLi Jian - The 2025 World Allergy Organization (WAO) Guidelines for the Classification, Diagnosis, and Treatment of Hereditary Angioedema (HAE) with Consideration of Worldwide Disparities provide a comprehensive, evidence-informed, and globally applicable framework for the care of this rare and potentially life-threatening disorder. HAE is a genetic disease characterized by recurrent episodes of subcutaneous and submucosal swelling, most commonly mediated by bradykinin, and is associated with substantial morbidity, impaired quality of life, and a lifelong risk of fatal laryngeal edema. The Guidelines were developed by an international panel of 40 experts from 22 countries, with representation from all world regions, reflecting the commitment of WAO to geographic diversity, inclusiveness, and global relevance. The development process for these guidelines followed a structured and transparent methodology that integrated systematic literature review, appraisal of real-world evidence, and application of the Grading of Recommendations, Assessment, Development and Evaluation (GRADE) framework adapted for rare diseases, complemented by a formal Delphi consensus process. This approach was specifically designed to address the limitations of conventional evidence hierarchies in rare disorders, while ensuring clinical applicability across heterogeneous healthcare systems and resource settings. A central element of the guidelines is an updated classification of HAE based on underlying pathophysiology and disease endotypes. The traditional distinction between HAE types 1 and 2 is unified under the term HAE with C1 inhibitor deficiency (HAE-C1-INH), reflecting shared biological mechanisms and management principles. The guidelines also recognize an expanding spectrum of HAE with normal C1 inhibitor (HAE-nC1-INH), including forms associated with pathogenic variants in F12, PLG, ANGPT1, KNG1, MYOF, HS3ST6, CPN1, and DAB2IP, as well as cases with currently unidentified genetic causes. The diagnostic strategy emphasizes early clinical recognition based on characteristic features, including recurrent angioedema without urticaria, abdominal or laryngeal involvement, early symptom onset, and family history. A simplified diagnostic algorithm is proposed, prioritizing the C1 inhibitor functional assay as the preferred initial test when performed in a reliable specialized laboratory. Alternative diagnostic pathways are outlined for settings with limited access to specialized testing, including pragmatic combinations of biochemical assays and selective use of genetic testing, particularly relevant for HAE-nC1-INH and family screening. Management recommendations address on-demand treatment of acute attacks, short-term prophylaxis, and individualized long-term prophylaxis. Universal access to on-demand therapy is emphasized for all patients with confirmed HAE, including those who are asymptomatic, given the unpredictable nature of attacks and lifelong risk. Long-term prophylaxis is addressed within a treat-to-target framework aimed at achieving complete disease control and sustained improvement in health-related quality of life, with regular reassessment and shared decision-making. Empowering patients and caregivers through structured education, access to appropriate medications, and integration with specialized referral centers is associated with earlier treatment, reduced healthcare utilization, and improved equity of care and reduced avoidable morbidity and mortality worldwide. The 2025 WAO Guidelines for Hereditary Angioedema establish an evidence-informed, patient-centered, and forward-looking framework for the classification, diagnosis, and management of HAE. By integrating advances in pathophysiology, diagnostics, and therapeutics with global expert consensus and real-world considerations, the guidelines aim to support consistent, equitable, and high-quality care for patients with HAE across regions and healthcare systems. - Source: PubMed
Publication date: 2026/03/19
Vázquez Daniel OGiavina-Bianchi PedroJosviack DaríoKaplan Allen PMartinez Pablo A SFantini ClaudioBernstein Jonathan AAbbas ShahidLevin Nancy AgmonAl-Ahmad MonaAlandijani SultanAlhashmi Hani AbdullahAli Ramzy MohammedAllam InesAl-Nesf Al-Mansouri MaryamAl-Tamemi SalemAltrichter SabineCastelló Mirta ÁlvarezAndoh Hilary DAun Marcelo VivoloMapondela Kassim BabuBanerji AleenaBara Noémi-AnnaBarrera Olga MelcinaPerigault Paulo BarreraBranco-Ferreira ManuelCalderón-Llosa Oscar ManuelCanonica Giorgio WalterAlmarales Raúl CastroCecchi LorenzoChang Yoon-SeokChantaphakul HiroshiChikovani TinatinChong-Neto Herberto JoseContreras-Verduzco Francisco AlbertoDefendi FedericaDorsainvil VilbrunEbisawa MotohiroEl-Sayed Zeinab AFasano Mary BethFazlollahi Mohammad RezaFemine EuguensFernandes Fátima RodriguesFiocchi AlessandroFonacier LuzGallego ClaudiaGarcía Abujeta José LuisGereda José EnriqueGiordano ErminiaGökmen Nihal MeteGómez R MaximilianoGonzalez MonicaDíaz Sandra GonzálezGrau MasumiHakl RomanHide MichihiroHossny ElhamHuilaja LauraHuq Syed RezaulIrani CarlaIshchanka AksanaIspayeva ZhanatJamalyan Kristina RKaidashev IgorKamkamidze GeorgeTanno Luciana KaseKathuria P CKessel AharonKiani-Alikhan SorenaKomarla Nagendra PrasadKvedarienė VioletaLang David MLee Yong WonLevin MichaelLi Philip HLi HenryLumry William RMachavariani KetevanMartinez-Sager InmaculadaMaselli Juan PMikos NikolaosMitskevich NunuMobayed Hassan M SMonge Ortega Olga PatriciaMorita HideakiMunkhbayarlakh SonomjamtsNabavi MohammadNaqvi Muhammad RazaOcampo JaimeOlivares MargaritaOrtega-Martell Jose AntonioOyuntsatsral BatsaikhanPapadopoulos NikosPatella VincenzoPawankar RubyPeter JonnyPsarros FotisRegateiro FredericoReidl MarcRigalt Ann MRincón Fernández Jenny MarielRivera Gómez Maria AntoniaRojo Gutiérrez María IsabelSahiner Ümit MuratSandoval-Ruballos MónicaSantos NatachaSarrazola MauricioSchrijvers RikShchurok IrynaSheikh Farrukh RafiqueSobotkova MartaSoria AngeleStefanaki EfthaliaTarazona RobinLuján Alejandra ValecillosRostan Marylin ValentinValerieva AnnaWing-Kin Wong GaryYong Patrick F KZaitoun FaresMartin Bryan LAnsotegui Ignacio JMorais-Almeida MárioCraig Timothy J - The Medical Device Related Pressure Injuries (MDRPIs) are a wound type that has been extensively tracked and recorded within observational studies, with a global patient prevalence of 19.3% [Zhang N et al. in Eur J Med Res 1:425, 2024] and 28.1% in acute care patients [Brophy S et al. in J Tissue Viability 4:489-498, 2021]. Yet, despite being an injury caused directly by medical intervention, to the author's knowledge, no in-depth proteomic analysis in this wound type has been published previously. This study represents a novel proteomic analysis of clinical MDRPI samples providing initial characterization of a protein pathway significant to wound healing in the context of MDRPIs developed in an ICU setting (Fig. 1). To investigate the proteomic changes associated with the healing outcomes of medical device related pressure injuries through comprehensive proteome characterisation. Clinical wound fluid samples were collected from Intensive Care Unit (ICU) patients with MDRPIs. These samples underwent analysis using Sequential Window Acquisition of all Theoretical Mass Spectra (SWATH-MS) mass spectrometry. The severity and healing trajectories of the injuries were assessed using the Pressure Ulcer Scale for Healing (PUSH) scores, facilitating the comparison of protein abundances to identify key pathways involved in healing and non-healing MDRPIs. The study identified a significant inverse correlation between the severity of non-healing MDRPIs and the levels of alpha-1 antitrypsin (A1AT) (R = -0.43; P = 0.035). A1AT functions as an inhibitor of neutrophil elastase (NE), which targets kininogen-1 (KNG-1). This relationship was further substantiated by a strong positive correlation between A1AT and KNG-1 levels (R = 0.76; Q < 6.8 × 10), indicating a protective function of A1AT over KNG-1 from NE. Given that KNG-1 contributes to early wound healing through its derivative, bradykinin, the misregulation of A1AT may disrupt the healing process of MDRPIs. The findings suggest that decreased levels of A1AT are associated with increased severity in non-healing MDRPIs, potentially due to the disruption of KNG-1 activity. These insights offer a foundation for further research into targeted therapeutic strategies aimed at enhancing the healing of MDRPIs. - Source: PubMed
Publication date: 2026/05/16
Fox Haydn ABroszczak Daniel ADoubrovsky AnnaLevido AnnabelPalmer JenniferCoyer FionaParker Tony J - Methotrexate (MTX)-induced liver injury (MTX-ILI) involves complex mechanisms that remain incompletely understood. This study investigated the role of NLR family pyrin domain containing 3 (NLRP3) inflammasome-mediated pyroptosis in MTX-ILI and explored the regulatory involvement of reactive oxygen species (ROS) and mitochondrial permeability transition pore (mPTP) opening. Wistar rats administered MTX and L02 cells exposed to MTX exhibited significant hepatocellular injury and pyroptotic features, as evidenced by elevated aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH), and Caspase-1 activities; increased interleukin-1β (IL-1β) and interleukin-18 (IL-18) levels; and upregulation of NLRP3, apoptosis-associated speck-like protein containing a CARD (ASC), gasdermin D (GSDMD), and its N-terminal fragment (GSDMD-N). These effects were attenuated by the NLRP3 inhibitor MCC950. In vitro, scavenging ROS with N-acetylcysteine (NAC) and inhibiting mPTP opening with ciclosporin A (CsA) markedly suppressed pyroptosis by alleviating mitochondrial dysfunction, reducing ROS accumulation, restoring mitochondrial membrane potential, and preserving mitochondrial ultrastructure. Label-free quantitative proteomics and protein-protein interaction analysis identified KNG1 and PARP12 as key proteins associated with ROS/mPTP-mediated pyroptosis, which were validated by Western blotting. Furthermore, Connectivity Map analysis predicted four potential therapeutic agents, including RS-127445, SB-218795, proadifen, and balicatib. Collectively, these findings demonstrate that MTX induces NLRP3-dependent pyroptosis through ROS accumulation and sustained mPTP opening. - Source: PubMed
Publication date: 2026/05/14
Cheng XuechunWu HaoZhuang XiupingYang BaohuiDing MingGao HongdaLi SijieLi QianWang Xin - Cerebral malaria (CM) due to ( ) infection is a major cause of death in African children. Bradykinin (BK) is a mediator of vasogenic edema. It could contribute to the pathogenesis of central nervous system malaria in Kenyan children and ANKA ( ) infected C57BL/6J mice with experimental cerebral malaria. Cleaved plasma high molecular weight kininogen (cHK) is a marker for prior BK release. 40% of children with central nervous system malaria had plasma cHK versus 18% of children with uncomplicated malaria. Wild-type -infected mice had circulating plasma cHK, elevated BK levels, and reduced HK and prekallikrein levels. HK null ( ), combined BK B1 and B2 receptor null ( ), BK B2 ( ) or BK B1 ( ) receptor null mice were protected from neurologic deterioration and brain edema compared to wild-type mice. mice were not protected from neurological deterioration. Prekallikrein null ( ), prolylcarboxypeptidase hypomorphs ( ), and brain endothelial cell conditional knockout of PRCP ( Cre) mice had reduced neurologic deterioration and brain edema. Adjuvant plasma kallikrein inhibition combined with artesunate treatment of -infected mice reversed neurologic deterioration and brain edema and prolonged survival relative to artesunate alone. BK-induced vasogenic edema contributes to human and murine CM. - Source: PubMed
Publication date: 2026/02/24
Pinheiro Alessandro de SaTeixeira Douglas ESilva-Aguiar Rodrigo PShim Young JunMerkulova Alona ASilbak SadiqSkomorovska-Prokvolit YelennaMidem DavidOgolla SidneyBurckhardt Bjoern BGangnus TanjaScharfstein JulioCaruso-Neves CelsoMcCarty Owen J TGailani DavidBader MichaelRosenthal Philip JDent Arlene EJanse Chris JMcCrae Keith RPinheiro Ana Acacia de SaKazura James WSchmaier Alvin H