HABP2

Last update 23 Jan 2025

Basic Info

Synonyms

Factor seven-activating protease, Factor VII-activating protease, FSAP

+ [12]

Introduction

Cleaves the alpha-chain at multiple sites and the beta-chain between 'Lys-53' and 'Lys-54' but not the gamma-chain of fibrinogen and therefore does not initiate the formation of the fibrin clot and does not cause the fibrinolysis directly. It does not cleave (activate) prothrombin and plasminogen but converts the inactive single chain urinary plasminogen activator (pro-urokinase) to the active two chain form. Activates coagulation factor VII (PubMed:8827452, PubMed:10754382, PubMed:11217080). May function as a tumor suppressor negatively regulating cell proliferation and cell migration (PubMed:26222560).

100 Clinical Results associated with HABP2

100 Translational Medicine associated with HABP2

0 Patents (Medical) associated with HABP2

435

Literatures (Medical) associated with HABP2

01 Nov 2024·The Journal of Nutrition

Diet, Microbiome, and Inflammation Predictors of Fecal and Plasma Short-Chain Fatty Acids in Humans

Article

Author: Newman, John W. ; Stephensen, Charles B ; Kable, Mary E ; Lemay, Danielle G ; Oliver, Andrew ; Kable, Mary E. ; Lemay, Danielle G. ; Stephensen, Charles B. ; Alkan, Zeynep ; Newman, John W

BACKGROUNDGut microbes produce short-chain fatty acids (SCFAs), which are associated with broad health benefits. However, it is not fully known how diet and/or the gut microbiome could be modulated to improve SCFA production.OBJECTIVESThe objective of this study was to identify dietary, inflammatory, and/or microbiome predictors of SCFAs in a cohort of healthy adults.METHODSSCFAs were measured in fecal and plasma samples from 359 healthy adults in the United States Department of Agriculture Nutritional Phenotyping Study. Habitual and recent diet was assessed using a Food Frequency Questionnaire and Automated Self-Administered 24-h Dietary Assesment Tool dietary recalls. Markers of systemic and gut inflammation were measured in fecal and plasma samples. The gut microbiome was assessed using shotgun metagenomics. Using statistics and machine learning, we determined how the abundance and composition of SCFAs varied with measures of diet, inflammation, and the gut microbiome.RESULTSWe show that fecal pH may be a good proxy for fecal SCFA abundance. A higher Healthy Eating Index for a habitual diet was associated with a compositional increase in fecal butyrate relative to acetate and propionate. SCFAs were associated with markers of subclinical gastrointestinal (GI) inflammation. Fecal SCFA abundance was inversely related to plasma lipopolysaccharide-binding protein. When we analyzed hierarchically organized diet and microbiome data with taxonomy-aware algorithms, we observed that diet and microbiome features were far more predictive of fecal SCFA abundances compared to plasma SCFA abundances. The top diet and microbiome predictors of fecal butyrate included potatoes and the thiamine biosynthesis pathway, respectively.CONCLUSIONSThese results suggest that resistant starch in the form of potatoes and microbially produced thiamine provide a substrate and essential cofactor, respectively, for butyrate synthesis. Thiamine may be a rate-limiting nutrient for butyrate production in adults. Overall, these findings illustrate the complex biology underpinning SCFA production in the gut. This trial was registered at clinicaltrials.gov as NCT02367287.

01 Nov 2024·The Journal of Nutrition

Fine-Scale Dietary Polyphenol Intake Is Associated with Systemic and Gastrointestinal Inflammation in Healthy Adults

Article

Author: Alkan, Zeynep ; Wilson, Stephanie M.G. ; Oliver, Andrew ; Stephensen, Charles B. ; Lemay, Danielle G. ; Awika, Joseph M ; Naveja, José J ; Lemay, Danielle G ; Larke, Jules A ; Wilson, Stephanie Mg ; Naveja, José J. ; Wilson, Stephanie MG ; Stephensen, Charles B ; Awika, Joseph M. ; Larke, Jules A.

BACKGROUNDPolyphenols are dietary bioactive compounds, many of which have anti-inflammatory properties. However, information on the intake of dietary polyphenols at the class and compound levels and their associations with gastrointestinal (GI) and systemic inflammation is lacking.OBJECTIVESEstimate dietary polyphenol intake in healthy adults and examine its relationship with GI and systemic inflammation markers.METHODSHealthy adults (n = 350) completed the United States Department of Agriculture Nutritional Phenotyping Study, an observational, cross-sectional study balanced for age, sex, and body mass index. Dietary intake, assessed via multiple 24-h recalls, was ingredientized and mapped to FooDB, a comprehensive food composition database. Dietary polyphenol intake (total, class, compound) was estimated and examined for its relationship to GI and systemic inflammation markers using linear models and random forest regressions.RESULTSMean total polyphenol intake was ∼914 mg/1000 kcal/d with flavonoids as the greatest class contributor (495 mg/1000 kcal/d). Tea, coffee, and fruits were among the largest food contributors to polyphenol intake. Total polyphenol intake was negatively associated with the GI inflammation marker, fecal calprotectin (β = -0.004, P = 0.04). At the class level, polyphenols categorized as prenol lipids (β = -0.94, P < 0.01) and phenylpropanoic acids (β = -0.92, P < 0.01) were negatively associated with plasma lipopolysaccharide-binding protein, a proxy for GI permeability. Food sources of these two classes included mainly olive products. We further detected a positive association between C-reactive protein and polyphenols in the "cinnamic acids and derivatives" class using hierarchical feature engineering and random forest modeling.CONCLUSIONSEven in healthy adults, dietary polyphenol intake was negatively associated with GI inflammation and intake of prenol lipids and phenylpropanoic acids was negatively associated with GI permeability. Relationships between polyphenol intake and inflammatory outcomes varied with the resolution-total, class, compound-of polyphenol intake, suggesting a nuanced impact of polyphenols on GI and systemic inflammation. This trial was registered at clinicaltrials.gov as NCT02367287.

01 Sep 2024·Acta Biomaterialia

CD44-hyaluronan mediating endocytosis of iron-platinum alloy nanoparticles induces ferroptotic cell death in mesenchymal-state lung cancer cells with tyrosine kinase inhibitor resistance

Article

Author: Lai, Yuhsuan ; Huang, Yuhsuan ; Chen, Helen Hw ; Su, Wuchou ; Wu, Shangyin ; Tsai, Tsunglin ; Wang, Hsiuyun ; Hou, Paosheng

While tyrosine kinase inhibitor resistance in cancer is a critical issue in the medical field, it is important for clinical testing as well, since it affects the ultimate outcome of cancer therapy. Yet, no effective solutions have been implemented till date. Clinical observations after tyrosine kinase inhibitor treatment reveal that acquired resistance inevitably limits the curative effects of non-small cell lung cancer treatment because of mutations in the epidermal growth factor receptor gene, which are accompanied by epithelial-mesenchymal transition. Here, for the first time, we report that the transmembrane glycoprotein CD44, which is associated with epithelial-mesenchymal transition, chemoresistance, and cancer progression, mediates enhanced endocytosis of iron-platinum alloy nanoparticles (FePt NPs) in the mesenchymal-state gefitinib-resistant (GR+ and M6) cells, via the binding of the CD44 ligand, hyaluronan, to the surface-absorbed hyaluronan-binding protein 2. Upon treatment with FePt NPs, there was higher cellular uptake in mesenchymal-state GR+ and M6 cells, resulting from cell death through ferroptosis and mitochondrial dysfunction, as compared to that observed in the epithelial-state cells. Mechanistically, inactivation of dihydroorotate dehydrogenase elevated the production of mitochondrial lipid peroxidation, and enhanced the cell death in the epithelial-state HCC827 cells, thereby indicating its role in defense against FePt NPs-induced ferroptosis. Furthermore, induction of ferroptosis has been shown to specifically promote the cell death of drug-tolerant "persister" cells and reverse their resistance as well. Therefore, we concluded that FePt NPs preferentially target mesenchymal drug-tolerant "persister" cells and promote ferroptosis, to overcome their resistance. STATEMENT OF SIGNIFICANCE: In the present study, we identified FePt NPs as an innovative agent for cancer treatment, particularly in mesenchymal-state cells that exhibit TKI resistance. Mesenchymal-state cancer cells showed enhanced uptake of FePt NPs via CD44-HA-mediated endocytosis, accompanied by severe cell death and mitochondrial morphology alterations, in comparison to epithelial-state cells. We further elucidated the mechanism underlying FePt NPs-induced ferroptotic cell death as via a burst of mitochondrial LPO and DHODH protein inactivation. In addition, we found that FePt NPs inhibit tumor growth in TKI-resistant mesenchymal GR+ cell-bearing mice with better efficacy than the ferroptotic inducer RSL3. Our current findings on using FePt NPs to overcome TKI resistance through ferroptosis activation may offer a alternative strategy for improved cancer treatment.

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HABP2

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