Dates of funding: 2020-2022
My research interests lie in understanding to the contribution of endoplasmic reticulum (ER) health and unfolded protein response (UPR) in maintaining skeletal homeostasis in physiologic and pathological conditions. I have broad background and training in the domains of genetics, molecular biology, microscopy, skeletal biology and mechanistic studies in osteoporosis. I have extensive experience in generating and leveraging conditional mice knockouts relevant for studying mechanisms of bone loss in osteoblast lineage cells. During my post-doctoral training, I focused on understanding mechanisms that mediate bone loss with sex steroid deficiency and age and role of senescence as their mediator. Specifically, I examined the role of FoxO family of transcription factors and sex hormones and their receptors in skeleton in particularly in osteoblast progenitor cells. As a faculty at University of Arkansas Medical Sciences, I generated genetic mouse models to specifically address the role of UPR sensors in osteoblast lineage cells and bone health. I was funded by P20 NIGMS COBRE project as junior PI in Arkansas for one year, during which I developed expertise in various microscopy techniques for imaging bone including TEM to visualize ER of osteoblasts on tissue sections. In the context of this proposal, I will focus on the effects of high-fat diet on osteoblast progenitor cells and actions of the UPR sensor Perk in these cells as a contributor to obesity-related skeletal changes. The present application leverages my strong background in osteoblast biology to examine the role of fundamental cellular pathways to define the molecular basis of skeletal fragility in setting of obesity.

Dates of funding: 2020-2022
My research interests lie in understanding to the contribution of endoplasmic reticulum (ER) health and unfolded protein response (UPR) in maintaining skeletal homeostasis in physiologic and pathological conditions. I have broad background and training in the domains of genetics, molecular biology, microscopy, skeletal biology and mechanistic studies in osteoporosis. I have extensive experience in generating and leveraging conditional mice knockouts relevant for studying mechanisms of bone loss in osteoblast lineage cells. During my post-doctoral training, I focused on understanding mechanisms that mediate bone loss with sex steroid deficiency and age and role of senescence as their mediator. Specifically, I examined the role of FoxO family of transcription factors and sex hormones and their receptors in skeleton in particularly in osteoblast progenitor cells. As a faculty at University of Arkansas Medical Sciences, I generated genetic mouse models to specifically address the role of UPR sensors in osteoblast lineage cells and bone health. I was funded by P20 NIGMS COBRE project as junior PI in Arkansas for one year, during which I developed expertise in various microscopy techniques for imaging bone including TEM to visualize ER of osteoblasts on tissue sections. In the context of this proposal, I will focus on the effects of high-fat diet on osteoblast progenitor cells and actions of the UPR sensor Perk in these cells as a contributor to obesity-related skeletal changes. The present application leverages my strong background in osteoblast biology to examine the role of fundamental cellular pathways to define the molecular basis of skeletal fragility in setting of obesity.

Dates of funding: 2020-2022
My research interests lie in understanding to the contribution of endoplasmic reticulum (ER) health and unfolded protein response (UPR) in maintaining skeletal homeostasis in physiologic and pathological conditions. I have broad background and training in the domains of genetics, molecular biology, microscopy, skeletal biology and mechanistic studies in osteoporosis. I have extensive experience in generating and leveraging conditional mice knockouts relevant for studying mechanisms of bone loss in osteoblast lineage cells. During my post-doctoral training, I focused on understanding mechanisms that mediate bone loss with sex steroid deficiency and age and role of senescence as their mediator. Specifically, I examined the role of FoxO family of transcription factors and sex hormones and their receptors in skeleton in particularly in osteoblast progenitor cells. As a faculty at University of Arkansas Medical Sciences, I generated genetic mouse models to specifically address the role of UPR sensors in osteoblast lineage cells and bone health. I was funded by P20 NIGMS COBRE project as junior PI in Arkansas for one year, during which I developed expertise in various microscopy techniques for imaging bone including TEM to visualize ER of osteoblasts on tissue sections. In the context of this proposal, I will focus on the effects of high-fat diet on osteoblast progenitor cells and actions of the UPR sensor Perk in these cells as a contributor to obesity-related skeletal changes. The present application leverages my strong background in osteoblast biology to examine the role of fundamental cellular pathways to define the molecular basis of skeletal fragility in setting of obesity.

Dates of funding: 2020-2022
My research interests lie in understanding to the contribution of endoplasmic reticulum (ER) health and unfolded protein response (UPR) in maintaining skeletal homeostasis in physiologic and pathological conditions. I have broad background and training in the domains of genetics, molecular biology, microscopy, skeletal biology and mechanistic studies in osteoporosis. I have extensive experience in generating and leveraging conditional mice knockouts relevant for studying mechanisms of bone loss in osteoblast lineage cells. During my post-doctoral training, I focused on understanding mechanisms that mediate bone loss with sex steroid deficiency and age and role of senescence as their mediator. Specifically, I examined the role of FoxO family of transcription factors and sex hormones and their receptors in skeleton in particularly in osteoblast progenitor cells. As a faculty at University of Arkansas Medical Sciences, I generated genetic mouse models to specifically address the role of UPR sensors in osteoblast lineage cells and bone health. I was funded by P20 NIGMS COBRE project as junior PI in Arkansas for one year, during which I developed expertise in various microscopy techniques for imaging bone including TEM to visualize ER of osteoblasts on tissue sections. In the context of this proposal, I will focus on the effects of high-fat diet on osteoblast progenitor cells and actions of the UPR sensor Perk in these cells as a contributor to obesity-related skeletal changes. The present application leverages my strong background in osteoblast biology to examine the role of fundamental cellular pathways to define the molecular basis of skeletal fragility in setting of obesity.

Dates of funding: 2020-2022
My research interests lie in understanding to the contribution of endoplasmic reticulum (ER) health and unfolded protein response (UPR) in maintaining skeletal homeostasis in physiologic and pathological conditions. I have broad background and training in the domains of genetics, molecular biology, microscopy, skeletal biology and mechanistic studies in osteoporosis. I have extensive experience in generating and leveraging conditional mice knockouts relevant for studying mechanisms of bone loss in osteoblast lineage cells. During my post-doctoral training, I focused on understanding mechanisms that mediate bone loss with sex steroid deficiency and age and role of senescence as their mediator. Specifically, I examined the role of FoxO family of transcription factors and sex hormones and their receptors in skeleton in particularly in osteoblast progenitor cells. As a faculty at University of Arkansas Medical Sciences, I generated genetic mouse models to specifically address the role of UPR sensors in osteoblast lineage cells and bone health. I was funded by P20 NIGMS COBRE project as junior PI in Arkansas for one year, during which I developed expertise in various microscopy techniques for imaging bone including TEM to visualize ER of osteoblasts on tissue sections. In the context of this proposal, I will focus on the effects of high-fat diet on osteoblast progenitor cells and actions of the UPR sensor Perk in these cells as a contributor to obesity-related skeletal changes. The present application leverages my strong background in osteoblast biology to examine the role of fundamental cellular pathways to define the molecular basis of skeletal fragility in setting of obesity.

Dates of funding: 2020-2022
My research interests lie in understanding to the contribution of endoplasmic reticulum (ER) health and unfolded protein response (UPR) in maintaining skeletal homeostasis in physiologic and pathological conditions. I have broad background and training in the domains of genetics, molecular biology, microscopy, skeletal biology and mechanistic studies in osteoporosis. I have extensive experience in generating and leveraging conditional mice knockouts relevant for studying mechanisms of bone loss in osteoblast lineage cells. During my post-doctoral training, I focused on understanding mechanisms that mediate bone loss with sex steroid deficiency and age and role of senescence as their mediator. Specifically, I examined the role of FoxO family of transcription factors and sex hormones and their receptors in skeleton in particularly in osteoblast progenitor cells. As a faculty at University of Arkansas Medical Sciences, I generated genetic mouse models to specifically address the role of UPR sensors in osteoblast lineage cells and bone health. I was funded by P20 NIGMS COBRE project as junior PI in Arkansas for one year, during which I developed expertise in various microscopy techniques for imaging bone including TEM to visualize ER of osteoblasts on tissue sections. In the context of this proposal, I will focus on the effects of high-fat diet on osteoblast progenitor cells and actions of the UPR sensor Perk in these cells as a contributor to obesity-related skeletal changes. The present application leverages my strong background in osteoblast biology to examine the role of fundamental cellular pathways to define the molecular basis of skeletal fragility in setting of obesity.

Dates of funding: 2020-2022
My research interests lie in understanding to the contribution of endoplasmic reticulum (ER) health and unfolded protein response (UPR) in maintaining skeletal homeostasis in physiologic and pathological conditions. I have broad background and training in the domains of genetics, molecular biology, microscopy, skeletal biology and mechanistic studies in osteoporosis. I have extensive experience in generating and leveraging conditional mice knockouts relevant for studying mechanisms of bone loss in osteoblast lineage cells. During my post-doctoral training, I focused on understanding mechanisms that mediate bone loss with sex steroid deficiency and age and role of senescence as their mediator. Specifically, I examined the role of FoxO family of transcription factors and sex hormones and their receptors in skeleton in particularly in osteoblast progenitor cells. As a faculty at University of Arkansas Medical Sciences, I generated genetic mouse models to specifically address the role of UPR sensors in osteoblast lineage cells and bone health. I was funded by P20 NIGMS COBRE project as junior PI in Arkansas for one year, during which I developed expertise in various microscopy techniques for imaging bone including TEM to visualize ER of osteoblasts on tissue sections. In the context of this proposal, I will focus on the effects of high-fat diet on osteoblast progenitor cells and actions of the UPR sensor Perk in these cells as a contributor to obesity-related skeletal changes. The present application leverages my strong background in osteoblast biology to examine the role of fundamental cellular pathways to define the molecular basis of skeletal fragility in setting of obesity.

Dates of funding: 2020-2022
My research interests lie in understanding to the contribution of endoplasmic reticulum (ER) health and unfolded protein response (UPR) in maintaining skeletal homeostasis in physiologic and pathological conditions. I have broad background and training in the domains of genetics, molecular biology, microscopy, skeletal biology and mechanistic studies in osteoporosis. I have extensive experience in generating and leveraging conditional mice knockouts relevant for studying mechanisms of bone loss in osteoblast lineage cells. During my post-doctoral training, I focused on understanding mechanisms that mediate bone loss with sex steroid deficiency and age and role of senescence as their mediator. Specifically, I examined the role of FoxO family of transcription factors and sex hormones and their receptors in skeleton in particularly in osteoblast progenitor cells. As a faculty at University of Arkansas Medical Sciences, I generated genetic mouse models to specifically address the role of UPR sensors in osteoblast lineage cells and bone health. I was funded by P20 NIGMS COBRE project as junior PI in Arkansas for one year, during which I developed expertise in various microscopy techniques for imaging bone including TEM to visualize ER of osteoblasts on tissue sections. In the context of this proposal, I will focus on the effects of high-fat diet on osteoblast progenitor cells and actions of the UPR sensor Perk in these cells as a contributor to obesity-related skeletal changes. The present application leverages my strong background in osteoblast biology to examine the role of fundamental cellular pathways to define the molecular basis of skeletal fragility in setting of obesity.

Dates of funding: 2020-2022
My research interests lie in understanding to the contribution of endoplasmic reticulum (ER) health and unfolded protein response (UPR) in maintaining skeletal homeostasis in physiologic and pathological conditions. I have broad background and training in the domains of genetics, molecular biology, microscopy, skeletal biology and mechanistic studies in osteoporosis. I have extensive experience in generating and leveraging conditional mice knockouts relevant for studying mechanisms of bone loss in osteoblast lineage cells. During my post-doctoral training, I focused on understanding mechanisms that mediate bone loss with sex steroid deficiency and age and role of senescence as their mediator. Specifically, I examined the role of FoxO family of transcription factors and sex hormones and their receptors in skeleton in particularly in osteoblast progenitor cells. As a faculty at University of Arkansas Medical Sciences, I generated genetic mouse models to specifically address the role of UPR sensors in osteoblast lineage cells and bone health. I was funded by P20 NIGMS COBRE project as junior PI in Arkansas for one year, during which I developed expertise in various microscopy techniques for imaging bone including TEM to visualize ER of osteoblasts on tissue sections. In the context of this proposal, I will focus on the effects of high-fat diet on osteoblast progenitor cells and actions of the UPR sensor Perk in these cells as a contributor to obesity-related skeletal changes. The present application leverages my strong background in osteoblast biology to examine the role of fundamental cellular pathways to define the molecular basis of skeletal fragility in setting of obesity.