Kallikrein-Related Peptidases 6 and 10 Are Elevated in Cerebrospinal Fluid
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G C A T T A C G G C A T genes Article Molecular Pathways Associated with Kallikrein 6 Overexpression in Colorectal Cancer Ritu Pandey 1,2,*, Muhan Zhou 3, Yuliang Chen 3, Dalila Darmoul 4 , Conner C. Kisiel 2, Valentine N. Nfonsam 5 and Natalia A. Ignatenko 1,2 1 Department of Cellular and Molecular Medicine, University of Arizona, Tucson, AZ 85721, USA; [email protected] 2 University of Arizona Cancer Center, University of Arizona, Tucson, AZ 85724, USA; [email protected] 3 Bioinformatics Shared Resource, University of Arizona Cancer Center, Tucson, AZ 85724, USA; [email protected] (M.Z.); [email protected] (Y.C.) 4 Institut National de la Santé et de la Recherche Médicale (INSERM), Université de Paris, Lariboisière Hospital, 75010 Paris, France; [email protected] 5 Department of Surgery, Section of Surgical Oncology, University of Arizona, Tucson, AZ 85724, USA; [email protected] * Correspondence: [email protected] Abstract: Colorectal cancer (CRC) remains one of the leading causes of cancer-related death world- wide. The high mortality of CRC is related to its ability to metastasize to distant organs. The kallikrein-related peptidase Kallikrein 6 (KLK6) is overexpressed in CRC and contributes to cancer cell invasion and metastasis. The goal of this study was to identify KLK6-associated markers for the CRC prognosis and treatment. Tumor Samples from the CRC patients with significantly elevated Citation: Pandey, R.; Zhou, M.; Chen, KLK6 transcript levels were identified in the RNA-Seq data from Cancer Genome Atlas (TCGA) Y.; Darmoul, D.; Kisiel, C.C.; and their expression profiles were evaluated using Gene Ontology (GO), Phenotype and Reactome Nfonsam, V.N.; Ignatenko, N.A. -
Kallikrein 13: a New Player in Coronaviral Infections
bioRxiv preprint doi: https://doi.org/10.1101/2020.03.01.971499; this version posted March 2, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. 1 Kallikrein 13: a new player in coronaviral infections. 2 3 Aleksandra Milewska1,2, Katherine Falkowski2, Magdalena Kalinska3, Ewa Bielecka3, 4 Antonina Naskalska1, Pawel Mak4, Adam Lesner5, Marek Ochman6, Maciej Urlik6, Jan 5 Potempa2,7, Tomasz Kantyka3,8, Krzysztof Pyrc1,* 6 7 1 Virogenetics Laboratory of Virology, Malopolska Centre of Biotechnology, Jagiellonian 8 University, Gronostajowa 7a, 30-387 Krakow, Poland. 9 2 Microbiology Department, Faculty of Biochemistry, Biophysics and Biotechnology, 10 Jagiellonian University, Gronostajowa 7, 30-387 Krakow, Poland. 11 3 Laboratory of Proteolysis and Post-translational Modification of Proteins, Malopolska 12 Centre of Biotechnology, Jagiellonian University, Gronostajowa 7a, 30-387 Krakow, 13 Poland. 14 4 Department of Analytical Biochemistry, Faculty of Biochemistry, Biophysics and 15 Biotechnology, Jagiellonian University, Gronostajowa 7 St., 30-387, Krakow, Poland. 16 5 University of Gdansk, Faculty of Chemistry, Wita Stwosza 63, 80-308 Gdansk, Poland. 17 6 Department of Cardiac, Vascular and Endovascular Surgery and Transplantology, Medical 18 University of Silesia in Katowice, Silesian Centre for Heart Diseases, Zabrze, Poland. 19 7 Centre for Oral Health and Systemic Diseases, University of Louisville School of Dentistry, 20 Louisville, KY 40202, USA. 21 8 Broegelmann Research Laboratory, Department of Clinical Science, University of Bergen, 22 5020 Bergen, Norway 23 24 25 26 27 28 29 30 31 * Correspondence should be addressed to Krzysztof Pyrc ([email protected]), Virogenetics 32 Laboratory of Virology, Malopolska Centre of Biotechnology, Jagiellonian University, 33 Gronostajowa 7, 30-387 Krakow, Poland; Phone number: +48 12 664 61 21; www: 34 http://virogenetics.info/. -
Aberrant Human Tissue Kallikrein Levels in the Stratum Corneum and Serum of Patients with Psoriasis: Dependence on Phenotype, Severity and Therapy N
CLINICAL AND LABORATORY INVESTIGATIONS DOI 10.1111/j.1365-2133.2006.07743.x Aberrant human tissue kallikrein levels in the stratum corneum and serum of patients with psoriasis: dependence on phenotype, severity and therapy N. Komatsu,* à K. Saijoh,§ C. Kuk,* F. Shirasaki,à K. Takeharaà and E.P. Diamandis* *Department of Pathology and Laboratory Medicine, Mount Sinai Hospital, Toronto, Ontario M5G 1X5, Canada Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ontario M5G 1L5, Canada àDepartment of Dermatology and §Department of Hygiene, Graduate School of Medical Science, School of Medicine, Kanazawa University, Kanazawa, Japan Summary Correspondence Background Human tissue kallikreins (KLKs) are a family of 15 trypsin-like or Eleftherios P. Diamandis. chymotrypsin-like secreted serine proteases (KLK1–KLK15). Multiple KLKs have E-mail: [email protected] been quantitatively identified in normal stratum corneum (SC) and sweat as can- didate desquamation-related proteases. Accepted for publication 7 November 2006 Objectives To quantify KLK5, KLK6, KLK7, KLK8, KLK10, KLK11, KLK13 and KLK14 in the SC and serum of patients with psoriasis, and their variation Key words between lesional and nonlesional areas and with phenotype, therapy and severity. diagnostic marker, human kallikreins, psoriasis, The overall SC serine protease activities were also measured. serine proteases, stratum corneum, therapy Methods Enzyme-linked immunosorbent assays and enzymatic assays were used. Conflicts of interest Results The lesional SC of psoriasis generally contained significantly higher levels None declared. of all KLKs. KLK6, KLK10 and KLK13 levels were significantly elevated even in the nonlesional SC. The overall trypsin-like, plasmin-like and furin-like activities were significantly elevated in the lesional SC. -
Human Tissue Kallikrein Expression in the Stratum Corneum and Serum of Atopic Dermatitis Patients
DOI:10.1111/j.1600-0625.2007.00562.x www.blackwellpublishing.com/EXD Original Article Human tissue kallikrein expression in the stratum corneum and serum of atopic dermatitis patients Nahoko Komatsu1,2,3,4, Kiyofumi Saijoh4, Cynthia Kuk1, Amber C. Liu1, Saba Khan1, Fumiaki Shirasaki3, Kazuhiko Takehara3 and Eleftherios P. Diamandis1,2 1Department of Pathology and Laboratory Medicine, Mount Sinai Hospital, Toronto, ON, Canada; 2Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON, Canada; 3Department of Dermatology, Graduate School of Medical Science, School of Medicine, Kanazawa University, Kanazawa, Japan; 4Department of Hygiene, Graduate School of Medical Science, School of Medicine, Kanazawa University, Kanazawa, Japan Correspondence: Eleftherios P. Diamandis, MD, PhD, FRCPC, Department of Pathology and Laboratory Medicine, Mount Sinai Hospital, 600 University Avenue, Toronto, ON M5G 1X5, Canada, Tel.: +1 416 586 8443, Fax: +1 416 586 8628, e-mail: [email protected] Accepted for publication 9 March 2007 Abstract: Human tissue kallikreins are a family of 15 trypsin- or differ significantly. In the serum of AD patients, KLK8 was chymotrypsin-like secreted serine proteases (KLK1–KLK15). Many significantly elevated and KLK5 and KLK11 were significantly KLKs have been identified in normal stratum corneum (SC) and decreased. However, their serum levels were not modified by sweat, and are candidate desquamation-related proteases. We corticosteroid topical agents. The alterations of KLK levels in the report quantification by enzyme-linked immunosorbent assay SC of AD were more pronounced than those in the serum. KLK7 (ELISA) of KLK5, KLK6, KLK7, KLK8, KLK10, KLK11, KLK13 and in the serum was significantly correlated with eosinophil counts in KLK14 in the SC and serum of atopic dermatitis (AD) patients by the blood of AD patients, while KLK5, KLK8 and KLK11 were ELISA, and examine their variation with clinical phenotype, significantly correlated with LDH in the serum. -
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Florida State University Libraries Faculty Publications The Department of Biomedical Sciences 2010 Functional Intersection of the Kallikrein- Related Peptidases (KLKs) and Thrombostasis Axis Michael Blaber, Hyesook Yoon, Maria Juliano, Isobel Scarisbrick, and Sachiko Blaber Follow this and additional works at the FSU Digital Library. For more information, please contact [email protected] Article in press - uncorrected proof Biol. Chem., Vol. 391, pp. 311–320, April 2010 • Copyright ᮊ by Walter de Gruyter • Berlin • New York. DOI 10.1515/BC.2010.024 Review Functional intersection of the kallikrein-related peptidases (KLKs) and thrombostasis axis Michael Blaber1,*, Hyesook Yoon1, Maria A. locus (Gan et al., 2000; Harvey et al., 2000; Yousef et al., Juliano2, Isobel A. Scarisbrick3 and Sachiko I. 2000), as well as the adoption of a commonly accepted Blaber1 nomenclature (Lundwall et al., 2006), resolved these two fundamental issues. The vast body of work has associated 1 Department of Biomedical Sciences, Florida State several cancer pathologies with differential regulation or University, Tallahassee, FL 32306-4300, USA expression of individual members of the KLK family, and 2 Department of Biophysics, Escola Paulista de Medicina, has served to elevate the importance of the KLKs in serious Universidade Federal de Sao Paulo, Rua Tres de Maio 100, human disease and their diagnosis (Diamandis et al., 2000; 04044-20 Sao Paulo, Brazil Diamandis and Yousef, 2001; Yousef and Diamandis, 2001, 3 Program for Molecular Neuroscience and Departments of 2003; -
Table S1. List of All Proteins Included in the Proseek® Multiplex Oncology I V2 96X96 Cancer Panel
Table S1. List of all proteins included in the Proseek® Multiplex Oncology I v2 96x96 Cancer Panel. Adrenomedullin (AM) Ezrin (EZR) Latency-associated peptide transforming growth factor beta-1 (LAP TGF-beta-1) Amphiregulin (AR) Fas antigen ligand (FasL) Angiopoietin-1 receptor (TIE2) FAS-associated death domain protein (FADD) Lipopolysaccharide-induced tumor necrosis factor- alpha factor (LITAF) B-cell activating factor (BAFF) Fms-related tyrosine kinase 3 ligand (Flt3L) Cadherin-3 (CDH3) Folate receptor alpha (FR-alpha) Macrophage colony-stimulating factor 1 (CSF-1) Carbonic anhydrase IX (CAIX) Follistatin (FS) Matrix metalloproteinase-1 (MMP-1) Carcinoembryonic antigen (CEA) Furin (FUR) Melanoma-derived growth regulatory protein (MIA) Caspase-3 (CASP-3) Growth hormone (GH) MHC class I polypeptide-related sequence A (MIC-A) C-C motif chemokine 19 (CCL19) Growth/differentiation factor 15 (GDF-15) Midkine (MK) CD40 ligand (CD40-L) Heparin-binding EGF-like growth factor (HB-EGF) Monocyte chemotactic protein 1 (MCP-1) C-X-C motif chemokine 5 (CXCL5) Hepatocyte growth factor (HGF) Myeloid differentiation primary response protein MyD88 (MYD88) C-X-C motif chemokine 9 (CXCL9) ICOS ligand (ICOSLG) C-X-C motif chemokine 10 (CXCL10) Immunoglobulin-like transcript 3 (ILT-3) NF-kappa-B essential modulator (NEMO) C-X-C motif chemokine 11 (CXCL11) Integrin alpha-1 (ITGA1) NT-3 growth factor receptor (NTRK3) C-X-C motif chemokine 13 (CXCL13) Interferon gamma (IFN-gamma) Ovarian cancer-related tumor marker CA 125 (CA-125) Cyclin-dependent kinase inhibitor -
Activation Profiles and Regulatory Cascades of the Human Kallikrein-Related Peptidases Hyesook Yoon
Florida State University Libraries Electronic Theses, Treatises and Dissertations The Graduate School 2008 Activation Profiles and Regulatory Cascades of the Human Kallikrein-Related Peptidases Hyesook Yoon Follow this and additional works at the FSU Digital Library. For more information, please contact [email protected] FLORIDA STATE UNIVERSITY COLLEGE OF ARTS AND SCIENCES ACTIVATION PROFILES AND REGULATORY CASCADES OF THE HUMAN KALLIKREIN-RELATED PEPTIDASES By HYESOOK YOON A Dissertation submitted to the Department of Chemistry and Biochemistry in partial fulfillment of the requirements for the degree of Doctor of Philosophy Degree Awarded: Fall Semester, 2008 The members of the Committee approve the dissertation of Hyesook Yoon defended on July 10th, 2008. ________________________ Michael Blaber Professor Directing Dissertation ________________________ Hengli Tang Outside Committee Member ________________________ Brian Miller Committee Member ________________________ Oliver Steinbock Committee Member Approved: ____________________________________________________________ Joseph B. Schlenoff, Chair, Department of Chemistry and Biochemistry The Office of Graduate Studies has verified and approved the above named committee members. ii ACKNOWLEDGMENTS I would like to dedicate this dissertation to my parents for all your support, and my sister and brother. I would also like to give great thank my advisor, Dr. Blaber for his patience, guidance. Without him, I could never make this achievement. I would like to thank to all the members in Blaber lab. They are just like family to me and I deeply appreciate their kindness, consideration and supports. I specially like to thank to Mrs. Sachiko Blaber for her endless guidance and encouragement. I would like to thank Dr Jihun Lee, Margaret Seavy, Rani and Doris Terry for helpful discussions and supports. -
A Predictive Model for Prostate Cancer Incorporating PSA Molecular Forms
www.nature.com/scientificreports OPEN A predictive model for prostate cancer incorporating PSA molecular forms and age Julia Oto1,5, Álvaro Fernández-Pardo1,5, Montserrat Royo1, David Hervás 2, Laura Martos1, César D. Vera-Donoso3, Manuel Martínez3, Mary J. Heeb4, Francisco España1, Pilar Medina1* & Silvia Navarro1* The diagnostic specifcity of prostate specifc antigen (PSA) is limited. We aimed to characterize eight anti-PSA monoclonal antibodies (mAbs) to assess the prostate cancer (PCa) diagnostic utility of diferent PSA molecular forms, total (t) and free (f) PSA and PSA complexed to α1-antichymotrypsin (complexed PSA). MAbs were obtained by immunization with PSA and characterized by competition studies, ELISAs and immunoblotting. With them, we developed sensitive and specifc ELISAs for these PSA molecular forms and measured them in 301 PCa patients and 764 patients with benign prostate hyperplasia, and analyzed their efectiveness to discriminate both groups using ROC curves. The free- to-total (FPR) and the complexed-to-total PSA (CPR) ratios signifcantly increased the diagnostic yield of tPSA. Moreover, based on model selection, we constructed a multivariable logistic regression model to predictive PCa that includes tPSA, fPSA, and age as predictors, which reached an optimism-corrected area under the ROC curve (AUC) of 0.86. Our model outperforms the predictive ability of tPSA (AUC 0.71), used in clinical practice. In conclusion, The FPR and CPR showed better diagnostic yield than tPSA. In addition, the PCa predictive model including age, fPSA and complexed PSA, outperformed tPSA detection efcacy. Our model may avoid unnecessary biopsies, preventing harmful side efects and reducing health expenses. -
The Physiology and Pathobiology of Human Kallikrein-Related Peptidase 6 (KLK6 )
Clin Chem Lab Med 2012;50(2):211–233 © 2012 by Walter de Gruyter • Berlin • Boston. DOI 10.1515/CCLM.2011.750 Review The physiology and pathobiology of human kallikrein-related peptidase 6 ( KLK6 ) Jane Bayani 1,2 and Eleftherios P. Diamandis 1 – 3, * surveys of normal and diseased genomes, transcriptomes, 1 Department of Laboratory Medicine and Pathobiology , proteomes and metabolomes. However, few, if any, biomark- University of Toronto, Toronto, ON, Canada ers have made their way to the clinic. Meanwhile, some FDA- 2 Samuel Lunenfeld Research Institute , Joseph and Wolf approved biomarkers are not used in standard clinical practice Lebovic Health Centre and Mt. Sinai Hospital, Toronto, and labelled as “ analyte-specifi c reagents (ASRs) ” , recom- ON, Canada mended for research purposes only (1) . Multiple biomarkers 3 Department of Clinical Biochemistry , Toronto General for disease diagnosis and personalised therapy are the way of Hospital, University Health Network, Toronto, ON , the future, but many still hope to fi nd simple biomarkers that Canada rival the likes of prostate specifi c antigen ( PSA ) for prostate cancer (2) . PSA , also known as kallikrein 3 ( KLK3 ), belongs to a unique family of 15 tissue kallikrein and kallikrein-related Abstract peptidase genes ( KLK s) (3 – 5) . Following the identifi cation The human kallikrein-related peptidase 6 ( KLK6 ) gene belongs of all human KLK family members in the late 1990s (6, 7) , to the 15-member kallikrein ( KLK ) gene family mapping to many investigators, including our group, have actively pur- chromosome 19q13.3 – 13.4. Encoding for an enzyme with sued the potential for other KLK family members as putative trypsin-like properties, KLK6 can degrade components of the biomarkers (3, 4) . -
Prognostic Significance of Multiple Kallikreins in High-Grade Astrocytoma Kristen L
Drucker et al. BMC Cancer (2015) 15:565 DOI 10.1186/s12885-015-1566-5 RESEARCH ARTICLE Open Access Prognostic significance of multiple kallikreins in high-grade astrocytoma Kristen L. Drucker1, Caterina Gianinni2, Paul A. Decker3, Eleftherios P. Diamandis4 and Isobel A. Scarisbrick1,5* Abstract Background: Kallikreins have clinical value as prognostic markers in a subset of malignancies examined to date, including kallikrein 3 (prostate specific antigen) in prostate cancer. We previously demonstrated that kallikrein 6 is expressed at higher levels in grade IV compared to grade III astrocytoma and is associated with reduced survival of GBM patients. Methods: In this study we determined KLK1, KLK6, KLK7, KLK8, KLK9 and KLK10 protein expression in two independent tissue microarrays containing 60 grade IV and 8 grade III astrocytoma samples. Scores for staining intensity, percent of tumor stained and immunoreactivity scores (IR, product of intensity and percent) were determined and analyzed for correlation with patient survival. Results: Grade IV glioma was associated with higher levels of kallikrein-immunostaining compared to grade III specimens. Univariable Cox proportional hazards regression analysis demonstrated that elevated KLK6- or KLK7-IR was associated with poor patient prognosis. In addition, an increased percent of tumor immunoreactive for KLK6 or KLK9 was associated with decreased survival in grade IV patients. Kaplan-Meier survival analysis indicated that patients with KLK6-IR < 10, KLK6 percent tumor core stained < 3, or KLK7-IR < 9 had a significantly improved survival. Multivariable analysis indicated that the significance of these parameters was maintained even after adjusting for gender and performance score. Conclusions: These data suggest that elevations in glioblastoma KLK6, KLK7 and KLK9 protein have utility as prognostic markers of patient survival. -
Kallikrein-Related Peptidase Signalling Via Proteinase-Activated Receptors
KALLIKREIN-RELATED PEPTIDASE SIGNALLING VIA PROTEINASE-ACTIVATED RECEPTORS by Aikaterini Oikonomopoulou A thesis submitted in conformity with the requirements for the Degree of Doctor of Philosophy Graduate Department of Laboratory Medicine and Pathobiology University of Toronto © Copyright by Aikaterini Oikonomopoulou 2008 Kallikrein-related peptidase signalling via proteinase-activated receptors Aikaterini Oikonomopoulou Doctor of Philosophy, 2008 Department of Laboratory Medicine and Pathobiology University of Toronto ABSTRACT The family of human kallikrein-related peptidases (KLKs) numbers 15 serine proteinases implicated in tumour progression. Despite the wide tissue distribution of KLKs and the numerous reports of their differential expression in pathological settings, the signalling mechanism(s) whereby these enzymes regulate tissue function are not yet known. Further, knowledge of the levels of their activity, as well as of their potential endogenous targets, has only been extracted from in vitro studies and cell culture systems. We hypothesized that KLKs can trigger tumour signalling via proteinase-activated receptors (PARs), a family of G-protein-coupled receptors. To test our hypothesis, we evaluated the ability of KLKs 5, 6, and 14: to activate or prevent signalling via PARs 1, 2, and 4 in cells and tissues expressing these receptors. Further, we used a novel activity-based probe approach, coupled with conventional immunoassay (ELISA), to determine the abundance of active KLK6 relative to total immunoreactive KLK6 in cancer-related biological fluids. We concluded that KLKs can regulate multiple signalling pathways triggered by PARs 1, 2, and 4, resulting in calcium release, platelet aggregation and vascular relaxation, and they can cause murine inflammation. Further, our activity-based ELISA demonstrated the presence of active KLK6 in ovarian cancer ascites fluids and cancer cell supernatants. -
Is Generation of C3(H2O) Necessary for Activation of the Alternative Pathway T in Real Life? ⁎ Kristina N
Molecular Immunology 114 (2019) 353–361 Contents lists available at ScienceDirect Molecular Immunology journal homepage: www.elsevier.com/locate/molimm Is generation of C3(H2O) necessary for activation of the alternative pathway T in real life? ⁎ Kristina N. Ekdahla,b, , Camilla Mohlinb, Anna Adlera, Amanda Åmana, Vivek Anand Manivela, Kerstin Sandholmb, Markus Huber-Langc, Karin Fromella, Bo Nilssona a Department of Immunology, Genetics and Pathology, Rudbeck Laboratory, Uppsala, Sweden b Linnaeus Center of Biomaterials Chemistry, Linnaeus University, Kalmar, Sweden c Institute for Clinical and Experimental Trauma Immunology, University Hospital of Ulm, Ulm, Germany ARTICLE INFO ABSTRACT Keywords: In the alternative pathway (AP) an amplification loop is formed, which is strictly controlled by various fluid- Complement system phase and cell-bound regulators resulting in a state of homeostasis. Generation of the “C3b-like” C3(H2O) has C3(H2O) been described as essential for AP activation, since it conveniently explains how the initial fluid-phase AP Conformation convertase of the amplification loop is generated. Also, the AP has a status of being an unspecific pathway Analysis despite thorough regulation at different surfaces. Proteases During complement attack in pathological conditions and inflammation, large amounts of C3b are formed by Alternative pathway the classical/lectin pathway (CP/LP) convertases. After the discovery of LP´s recognition molecules and its tight interaction with the AP, it is increasingly likely that the AP acts in vivo mainly as a powerful amplification mechanism of complement activation that is triggered by previously generated C3b molecules initiated by the binding of specific recognition molecules. Also in many pathological conditions caused by a dysregulated AP amplification loop such as paroxysmal nocturnal hemoglobulinuria (PNH) and atypical hemolytic uremic syndrome (aHUS), C3b is available due to minute LP and CP activation and/or generated by non-complement proteases.