HABP2

Last update 08 May 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:10754382, PubMed:11217080, PubMed:8827452). 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

383

Literatures (Medical) associated with HABP2

03 Mar 2025·Journal of Cancer

Clinical significance and immune landscape analyses of the coagulation-related gene signatures in gastric cancer

Article

Author: Huang, Xiaoping ; Zhou, Xiaojiang ; Feng, Zhou ; Liu, Dingwei ; Yu, Yueming ; Li, Hui ; Xie, Yong ; Xie, Jun

Gastric cancer (GC) is one of the most common types of clinically malignant tumors and a global health challenge due to its high mortality and poor prognosis. The coagulation cascade is closely related to GC and plays a key role in the tumor immune microenvironment. However, the specific mechanisms by which coagulation-related genes involved in the occurrence and development of GC remains unclear. The data of GC patients and coagulation-related genes were obtained from the TCGA and the GSEA databases, respectively. After univariate Cox regression analysis, the non-negative matrix factorization method was used to identify coagulation-related molecular subtypes. GC patients were categorized into high-risk and low-risk score groups based on median risk scores, which included six genes (PCDHAC1, HABP2, GPC3, GFRA1, F5, and DKK1). There was a significant difference in survival between the two groups, and the predictive abilities for 1-, 3-, and 5-year survival were valid. Here, we demonstrated that coagulation-related gene signatures are valuable in predicting the survival of GC patients. Besides, the high- and low-risk grouping also better reflects the status of tumor mutation burden and the characteristics of tumor immune infiltration in GC, which provides a theoretical basis for individualized chemotherapy and immunotherapy for GC patients.

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.

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HABP2

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