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Processing of VEGF-C and -D by the proprotein convertases : importance in angiogenesis, lymphangiogenesis, and tumorigenesis / Géraldine Siegfried and Abdel-Majid Khatib.
Morgan & Claypool Colloquium Collection 2 Available online
Morgan & Claypool Colloquium Collection 2- Format:
- Book
- Author/Creator:
- Siegfried, Géraldine, author.
- Khatib, A-Majid (Abdel-Majid), author.
- Series:
- Colloquium digital library of life sciences
- Colloquium series on protein activation and cancer ; 2169-9410 # 6.
- Colloquium series on protein activation and cancer, 2169-9410 ; # 6
- Language:
- English
- Subjects (All):
- Vascular endothelial growth factors.
- Proprotein convertases.
- Vascular Endothelial Growth Factors.
- Proprotein Convertases.
- Medical Subjects:
- Vascular Endothelial Growth Factors.
- Proprotein Convertases.
- Physical Description:
- 1 online resource (xi, 54 pages) : illustrations.
- Place of Publication:
- San Rafael, California (1537 Fourth Street, San Rafael, CA 94901 USA) : Morgan & Claypool, 2014.
- System Details:
- Mode of access: World Wide Web.
- text file
- Summary:
- The vascular endothelial growth factor (VEGF) family members that include VEGF-A, -B, -C, -D, and placental growth factor (PlGF), display distinct binding affinities for their receptors VEGFR-1, -2, and/or -3. In addition to their requirements in the initiation, development, and maintenance of blood and lymphatic vasculature, VEGFs and VEGFRs are upregulated during neoplasia and are involved in the remodeling of tumoral blood and lymphatic vasculature. By activating VEGFR-1 and VEGFR-2, both expressed on blood endothelial cells, VEGF-A promotes the formation of new tumoral blood vessels and thereby accelerates tumor growth. In contrast, upregulation of VEGF-C, a ligand for lymphatic endothelial VEGFR-3 as well as for VEGFR-2, induces the formation of tumor-associated lymphatic vessels and thus promotes the passive metastatic dissemination of tumor cells to regional lymph nodes. Of the VEGF family members, only VEGF-C and -D were found to be proteolytically processed by Furin-like enzymes. This processing controls the selective activation of VEGFR-2 and -3 signaling during tumor angiogenesis and lymphangiogenesis. Here, we provide an overview of angiogenesis processes and discuss the importance of VEGF-C and VEGF-D precursors processing by the proprotein convertases during the activation of VEGFR-2 and VEGFR-3 receptors and the mediation of their functions during angiogenesis, lymphangiogenesis, and tumorigenesis.
- Contents:
- Abbreviations
- Acknowledgments
- 1. Angiogenesis: a global overview
- 1.1 New vessels formation processes
- 1.1.1 Intussusception and sprouting angiogenesis
- 1.2 The vascular system
- 1.2.1 Structure of vascular system
- 1.3 The lymphatic system
- 1.3.1 Structure of lymphatic system
- 2. VEGF family members, their receptors, and signaling
- 2.1 Vascular endothelial growth factors (VEGFs)
- 2.2 Neuropilins
- 3. Activation, signaling, and function of VEGFRs
- 3.1 VEGFR1: a negative angiogenesis regulator
- 3.2 VEGFR2 receptor
- 3.2.1 Induction of proliferation by VEGF-A
- 3.2.2 Induction of migration by VEGF-R2 activation
- 3.2.3 Regulation of survival by VEGFR2 activation
- 3.2.4 Regulation of vascular permeability by VEGFR-2
- 3.3 VEGFR3 signaling and function
- 3.4 VEGFR heterodimerization
- 4. The role of VEGF family members in tumor angiogenesis and lymphangiogenesis
- 4.1 VEGFs and VEGFRs in tumor angiogenesis
- 4.2 VEGFs and VEGFRs in tumor-associated lymphangiogenesis
- 5. Maturation of VEGF-C and VEGF-D by the proprotein convertases
- 5.1 VEGF-C precursor processing by the proprotein convertases
- 5.1.1 ProVEGF-C processing by the PCs and normal angiogenesis: fin zebrafish model
- 5.1.2 Processing of ProVEGF-C in tumor angiogenesis and lymphangiogenesis
- 5.2 Processing of VEGF-D by the PCs
- 5.3 Concluding remarks
- References
- Author biographies.
- Notes:
- Part of: Colloquium digital library of life sciences.
- Title from PDF title page (viewed on December 23, 2013).
- Series from website.
- Includes bibliographical references (pages 37-51).
- ISBN:
- 9781615046119
- Access Restriction:
- Restricted for use by site license.
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