CV Lattes
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Universidade Federal de São Paulo (UNIFESP). Campus São Paulo. Escola Paulista de Medicina (EPM) (Institutional affiliation from the last research proposal) Birthplace: Brazil
Camila Lopes Veronez is graduated in Biomedicine at UNIFESP, completed her MSc and PhD in Molecular Biology at UNIFESP, and postdoc at the Max-Delbrück-Centrum für Molekulare Medizin, Berlin/Germany (2017-2018) and at UNIFESP (2018-2019). She worked as Assistant Project Scientist at Bruce Zuraw's lab at the Division of Rheumatology, Allergy and Immunology, UCSD from 2019-2021. She has experience in biochemistry/molecular biology, and human genetics, acting on the following subjects: kallikrein-kinin system, hereditary angioedema, and bradykinin-mediated angioedema. She has been working on animal models' establishment and gene editing in the topics of interest.Currently, works as scientific advisor in rare diseases at Sanofi, Brazil. (Source: Lattes Curriculum)
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Hereditary angioedema (HAE) is a rare genetic disease resulting from a deficiency of C1 inhibitor (C1-INH) or mutations in F12 gene. In both cases, the changes lead to uncontrolled activation of the kallikrein-kinin system (KKS) culminating in excessive release of bradykinin (BK). HAE profoundly affects the quality of life, treatment is expensive and often inefficient. We propose a gene t…
The hereditary angioedema (HAE) is characterized by repetitive episodes of painfuledemas and discomfort which affects mainly the upper and lower extremities, gastrointestinaltract, genitals and face, and it can lead to death by asphyxiation in swelling of upperrespiratory tract. The HAE is an autosomal-dominant disorder resulting from mutations in theC1 inhibitor that result in its abnorm…
Human plasma kallikrein-kinin system is formed by plasma kallikrein (huPK), which hydrolyzes its natural substrate high molecular weight kininogen (HK) and releases bradykinin (BK), and this system is related to vascular biology interacting with coagulation, fibrinolysis and complement systems.BK (RPPGFSPFR) can reproduce the characteristics of inflammatory state, such as the increase of …
Hereditary angioedema (HAE) is mainly known as an autosomal dominant disease characterized by C1 esterase inhibitor (C1-INH) deficiency. C1-INH inhibits proteases of the complement pathways, coagulation factors XI (FXI) and XII (FXII), plasma kallikrein (KK), and its deficiency results in an uncontrolled release of bradykinin (BK), which binds to the kinin B2 receptor (B2R) leading to inf…
Hereditary angioedema (HAE) is mainly known as an autosomal dominant disease characterized by C1 esterase inhibitor (C1-INH) quantitative (type I) or functional (type II) deficiency leading to swellings of one or more tissues. C1-INH inhibits proteases of the complement pathways, coagulation factors XI (FXI) and XII (FXII), plasma kallikrein (KK), and its deficiency results in an uncontro…
| 4 / 3 | Completed scholarships in Brazil |
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