Advanced search
Start date
Betweenand

MODULATION OF NCLX GENE EXPRESSION

Grant number: 22/03975-1
Support type:Scholarships in Brazil - Scientific Initiation
Effective date (Start): June 01, 2022
Effective date (End): May 31, 2023
Field of knowledge:Biological Sciences - Biochemistry - Metabolism and Bioenergetics
Principal researcher:Alicia Juliana Kowaltowski
Grantee:Julia Kühl Teles Martini
Home Institution: Instituto de Química (IQ). Universidade de São Paulo (USP). São Paulo , SP, Brazil
Associated research grant:20/06970-5 - Mitochondrial ion transporters as sensors and regulators in energy metabolism, AP.TEM

Abstract

Mitochondrial Ca2+ has an important role in physiology and pathology. Mitochondrial transporters are crucial to maintain Ca2+ homeostasis, and Ca2+ efflux is controlled by the mitochondrial Na+/ Ca2+/ Li+ Exchanger (NCLX).NCLX is important to many physiological cellular processes, such as mitochondrial matrix redox state maintenence, and in different tissues, including brown adipose tissue, sensory neurons, B lymphocytes, and cardiomyocytes. In addition to physiological states, NCLX is a prominent factor in pathological processes, such as in cardiac ischemia, Alzheimer's disease, and colorectal cancer. However, the factors regulating NCLX expression are still unknown. In this sense, the aim of this work is to explore the potential modulation of NCLX expression by mild cellular stress factors - serum deprivation, cytosolic calcium overload, and oxidants. NCLX expression will be monitored by the assessment of mRNA, protein levels, and activity. This work can contribute to a better understanding of NCLX modulation, considering that its expression and/or activity have been related to pathophysiologic processes, and is thus a potential therapeutic target.

News published in Agência FAPESP Newsletter about the scholarship:
Articles published in other media outlets (0 total):
More itemsLess items
VEICULO: TITULO (DATA)
VEICULO: TITULO (DATA)

Please report errors in scientific publications list by writing to: cdi@fapesp.br.