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Marioly Anneliese Muller Sobarzo

Académico

Universidad de Chile

Santiago, Chile

Líneas de Investigación


I am interested in exploring the mitochondrial Ca2+ regulation relieving the importance of mitochondrial Ca2+ dyshomeostasis and consequent Ca2+ overload as an early hallmark event in the pathophysiological process of several diseases.

Educación

  •  Doctora en Ciencias Biomédicas, UNIVERSIDAD DE CHILE. Chile, 2021
  •  Magister en Biología Celular, UNIVERSIDAD DE CHILE. Chile, 2009
  •  Licenciada en Tecnología Médica, UNIVERSIDAD DE CHILE. Chile, 2000
  •  Tecnólogo Médico, UNIVERSIDAD DE CHILE. Chile, 2000
  •  Educación en Ciencias de la Salud, UNIVERSIDAD DE CHILE. Chile, 2003

Experiencia Académica

  •   Profesor ayudante Part Time

    UNIVERSIDAD DE CHILE

    Medicina

    Santiago, Chile

    2001 - 2005

  •   Profesor instructor Part Time

    UNIVERSIDAD DE CHILE

    Medicina

    Santiago, Chile

    2005 - 2012

  •   Profesor asistente Full Time

    UNIVERSIDAD DE CHILE

    Medicina

    Santiago, Chile

    2013 - At present

  •   Subdirectora Full Time

    UNIVERSIDAD DE CHILE

    Medicina

    Santiago, Chile

    2018 - 2022

  •   Subdirectora Académica Part Time

    UNIVERSIDAD DE CHILE

    Medicina

    Santiago, Chile

    2022 - At present

Experiencia Profesional

  •   Asistente de investigación Part Time

    Universidad de Chile

    Santiago, Chile

    2001 - 2006

  •   Asistente de investigación Full Time

    Universidad de Pennsylvania

    Filadelfia, Estados Unidos

    2006 - 2012


 

Article (21)

HERPUD1 governs tumor cell mitochondrial function via inositol 1,4,5-trisphosphate receptor-mediated calcium signaling
Mitochondria and Calcium Regulation as Basis of Neurodegeneration Associated With Aging
Selective Vulnerability of Cancer Cells by Inhibition of Ca2+ Transfer from Endoplasmic Reticulum to Mitochondria (vol 14, pg 2313, 2016)
MCUR1 (ccdc90a) is a regulator of the mitochondrial calcium uniporter
Genetic identification of a role of InsP3 receptor-mediated exaggerated Ca2+ signaling in Alzheimer’s disease pathogenesis
Suppression of InsP<sub>3</sub> Receptor-Mediated Ca<SUP>2+</SUP> Signaling Alleviates Mutant Presenilin-Linked Familial Alzheimer's Disease Pathogenesis
MCUR1 is an essential component of mitochondrial Ca2+ uptake that regulates cellular metabolism.
MICU1 is an essential gatekeeper for MCU-mediated mitochondrial Ca(2+) uptake that regulates cell survival.
Constitutive cAMP response element binding protein (CREB) activation by Alzheimer's disease presenilin-driven inositol trisphosphate receptor (InsP3R) Ca2+ signaling.
Enhanced ROS generation mediated by Alzheimer's disease presenilin regulation of InsP3R Ca2+ signaling
Enhanced ROS Generation Mediated by Alzheimer's Disease Presenilin Regulation of InsP<sub>3</sub>R Ca<SUP>2+</SUP> Signaling
Essential regulation of cell bioenergetics by constitutive InsP3 receptor Ca2+ transfer to mitochondria.
Mechanism of Ca2+ Disruption in Alzheimer's Disease by Presenilin Regulation of InsP3 Receptor Channel Gating
Mechanism of Ca2+ disruption in Alzheimer’s disease by presenilin regulation of InsP3 receptor channel gating
Mechanism of Ca<SUP>2+</SUP> disruption in Alzheimer's disease by presenilin regulation of InsP<sub>3</sub> receptor channel gating
Calcium release by ryanodine receptors mediates hydrogen peroxide-induced activation of ERK and CREB phosphorylation in N2a cells and hippocampal neurons
Myotube depolarization generates reactive oxygen species through NAD(P)H oxidase; ROS-elicited Ca2+ stimulates ERK, CREB, early genes
Depolarization of skeletal muscle cells induces phosphorylation of cAMP response element binding protein via calcium and protein kinase C alpha
Depolarization-induced slow calcium transients activate early genes in skeletal muscle cells
Testosterone stimulates intracellular calcium release and mitogen-activated protein kinases via a G protein-coupled receptor in skeletal muscle cells
IP3 receptor function and localization in myotubes: an unexplored Ca2+ signaling pathway in skeletal muscle

Proyecto (1)

MITOCHONDRIA CA2 UPTAKE MEDIATED BY INSP3 RECEPTORS IS REQUIRED TO MAINTAIN CANCER CELL BIOENERGETICS. ITS INHIBITION RESULTS IN SELECTIVE CANCER CELL DEATH.

Review (2)

Natural killer T cells in allergic asthma: implications for the development of novel immunotherapeutical strategies
Targeting VCAM-1: a therapeutic opportunity for vascular damage
19
Marioly Muller

Académico

Tecnología Médica

Universidad de Chile

Santiago, Chile

6
Enrique Jaimovich

Full Professor

ICBM

FACULTAD DE MEDICINA, UNIVERSIDAD DE CHILE

Santiago, Chile

2
Gina Sanchez

Profesor Asociado

ICBM

UNIVERSIDAD DE CHILE, FAC MEDICINA , ICBM

Santiago, Chile

2
M. Cecilia Hidalgo

Professor

ICBM

Universidad de Chile

Santiago, Chile

2
Julio Cardenas

Associated Professor

Center for Integrative Biology

Universidad Mayor de Chile

Santiago, Chile

2
Berta Espinosa

Full Professor

Tecnología Médica

Universidad de Chile

Santiago, Chile

1
juan rios

asistente de laboratorio

fundacion cequa

punta arenas, Chile

1
Felipe Court

Full Professor and Director

Center for Integrative Biology

Universidad Mayor

Huechuraba, Chile

1
Mario Sanhueza

Regional Director of Research

Universidad Mayor

Temuco, Chile

1
Alenka Lovy

Assistant Professor

Science

Universidad Mayor de Chile

Santiago, Chile

1
Christian Gonzalez

Full Professor

Biology

Universidad de Chile

Santiago, Chile

1
Ulrike Kemmerling

Full Professor

ICBM

Facultad de Medicina, Universidad de Chile

Santiago, Chile

1
Maria Aylwin

Associate Professor

Universidad de Talca

Talca, Chile

1
ALEJANDRA SAN MARTIN

Professor

Medicine

Universidad Andrés Bello

Santiago, Chile

1
Pablo Muñoz

Profesor titular

Patología y Fisiología

UNIVERSIDAD DE VALPARAÍSO

Valparaiso, Chile

1
Fernanda Sanhueza

Bioquímica

Hospital Base San José de Osorno

Osorno, Chile