This assessment focuses on the molecular and cellular mechanisms of angiogenesis. It evaluates understanding of the transformation and expansion of blood vessels, the role of pericytes and tip cells, and the regulation of angiogenesis. Essential for students and professionals in biology and health sciences.
Capillary
Small venule
Smart arteriole
Capillaries and small venules
Capillaries and arteries
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Pericytes
Actin myosin filaments
Tip cells
Mesenchymal cells
None of the responses are correct
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Pericytes detach from the wall of a blood vessel, thus destabilizing it
The permeability of the blood vessel increases, causing proteases and stromal mix components to leak out
A tip cell extends itself out from the vessel into the stroma and guides the advancement of a new capillary sprout
Endothelial cells behind the tip cell replicate and form a stalk-like structure
None of the responses are correct
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Stromal cell
Pericyte
Mesenchymal cell
Stalk cell
Tip cell
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Tightly; maintaining a balance between adhesion molecules and colony-stimulating factors
Tightly; maintaining a balance between VEGF and TNF-α
Tightly; maintaining a balance between proangiogenic and antiangiogenic molecules
Poorly; maintaining a balance between proangiogenic and antiangiogenic molecules
loosely; maintaining a balance between proangiogenic and antiangiogenic molecules
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Placental growth factor (PlGF)
Platelet-derived growth factor (PDGF)
Vascular endothelial cell growth factor
Angiopoietin-1
All of the above are proangiogenic growth factors
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Colony stimulating factors
Growth factors
Adhesion molecules
Ang2
All of the above are proangiogenic factors
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Angiopoietin-2 (Ang 2), thrombospondins (TSP-1, TSP-2), tissue inhibitors of matrix matelloproteinases
Angiopoietin-2 (Ang 2), angiostatin, epidermal growth factor (EGF)
AvB3-integrin, angiostatin, endostatin
Angiopoietin-2 (Ang 2), thrombospondins (TSP-1, TSP-2), tissue inhibitors of matrix matelloproteinases, epidermal growth factor (EGF)
Angiopoietin-2 (Ang 2), tissue inhibitors of matrix matelloproteinases, AvB3-integrin, endostatin
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VEGF-A, VEGF-B, VEGF-C
VEGF-D, placental growth factor
Platelet-derived growth factor (PDGF)
VEGF-A, VEGF-B, VEGF-C, VEGF-D, placental growth factor
All of the responses are correct
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Tyrosine kinase
NR3C4
Neuropilins
Tyrosine kinases and neuropilins
All of the responses are correct
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VEGFR-1
VEGFR-2
Neuropilin-1
Neuropilin-2
All of the above
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VEGF-A
VEGF-B
VEGF-C
VEGF-D
VEGF-E
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VEGFR-1
VEGFR-2
Neuropilin-1
Neuropilin-2
Placental growth factor receptor (PlGF)
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VEGFR
NR3C4
Neuropilins
VEGFR and neuropilins
None of the responses are correct
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PDGFR-α
PDGFR-γ
PDGFR-δ
PDGFR-α and PDGFR- δ
None of the responses are correct
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True
False
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Cell migration
Cell replication
Cell survival
Cell migration, cell replication and cell survival
None of the responses are correct
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Monomers
Dimers
Trimers
Tetramers
Pentamers
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VEGF-A
VEGF-B
VEGF-C
VEGF-D
Placental growth factor
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It is involved in the regulation of cell growth.
It is involved in the regulation of cell proliferation.
It is involved in the regulation of cell survival.
It is involved in the regulation of cell growth and cell survival.
All of the responses are correct
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HIFα/mAKAP
MTOR
HIFα/VHL
HIFβ/VHL
HIFβ/mAKAP
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Proliferation of tumor cells
Migration of tumor cells
Growth of tumor cells
Protein synthesis and transcription
Proliferation and migration of tumor cells
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Increase in the ease with which tumor cells can enter blood vessels
Avoidance of immune system surveillance
Potential to decrease metastatic potential
Potential enhancement of immune system surveillance
Increase in the ease with which tumor cells can enter blood vessels as well as avoidance of immune system surveillance
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Decreased expression of antiangiogenic factors by tumor and stroma cells
Increased expression of proangiogenic proteins by tumor cells
Recruitment of endothelial cell precursors to the tumor microenvironment
Decreased expression of proangiogenic proteins by cells in the stroma surrounding the tumor
All of the responses are correct
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