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Protein kinase Cε targets respiratory chain and mitochondrial membrane potential but not F0F1‐ATPase in renal cells injured by oxidant

Journal of cellular biochemistry, 2018-11, Vol.119 (11), p.9394-9407

2018

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Protein kinase Cε targets respiratory chain and mitochondrial membrane potential but not F 0 F 1 -ATPase in renal cells injured by oxidant

Journal of cellular biochemistry, 2018-11, Vol.119 (11), p.9394-9407

2018

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Succinate ameliorates energy deficits and prevents dysfunction of complex I in injured renal proximal tubular cells

The Journal of pharmacology and experimental therapeutics, 2008-03, Vol.324 (3), p.1155-1162

2008

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Deletion of protein kinase C-ε attenuates mitochondrial dysfunction and ameliorates ischemic renal injury

American journal of physiology. Renal physiology, 2017-01, Vol.312 (1), p.F109-F120

2017

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Protein kinase C-α activation promotes recovery of mitochondrial function and cell survival following oxidant injury in renal cells

American journal of physiology. Renal physiology, 2012-08, Vol.303 (4), p.F515-F526

2012

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Protein Kinase C-α Interaction with F0F1-ATPase Promotes F0F1-ATPase Activity and Reduces Energy Deficits in Injured Renal Cells

The Journal of biological chemistry, 2015-03, Vol.290 (11), p.7054-7066

2015

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Deletion of protein kinase C-e attenuates mitochondrial dysfunction and ameliorates ischemic renal injury

American journal of physiology. Renal physiology, 2017-01, Vol.312 (1), p.F409

2017

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Protein kinase C-[alpha] activation promotes recovery of mitochondrial function and cell survival following oxidant injury in renal cells

American journal of physiology. Renal physiology, 2012-08, Vol.303 (4), p.F515

2012

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Protein kinase C-α activation promotes recovery of mitochondrial function and cell survival following oxidant injury in renal cells

American journal of physiology. Renal physiology, 2012, Vol.72 (2)

2012

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Protein kinase C-epsilon activation induces mitochondrial dysfunction and fragmentation in renal proximal tubules

American journal of physiology. Renal physiology, 2011-07, Vol.301 (1), p.F197-F208

2011

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Assessment of Mitochondrial Functions and Cell Viability in Renal Cells Overexpressing Protein Kinase C Isozymes

Journal of visualized experiments, 2013-01 (71)

2013

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γ-Tocotrienol protects against mitochondrial dysfunction and renal cell death

The Journal of pharmacology and experimental therapeutics, 2012-02, Vol.340 (2), p.330-338

2012

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Protein kinase C-[epsilon] activation induces mitochondrial dysfunction and fragmentation in renal proximal tubules

American journal of physiology. Renal physiology, 2011-07, Vol.301 (1), p.F197

2011

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Protein kinase C-ε activation induces mitochondrial dysfunction and fragmentation in renal proximal tubules

American journal of physiology. Renal physiology, 2011, Vol.70 (1)

2011

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Assessment of mitochondrial functions and cell viability in renal cells overexpressing protein kinase C isozymes

Journal of visualized experiments, 2013-01 (71)

2013

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The repair of Na+‐dependent glucose uptake following injury is regulated by PKC‐α and PKC‐ε

The FASEB journal, 2007-04, Vol.21 (5), p.A506-A506

2007

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Activation of ERK1/2 pathway mediates oxidant-induced decreases in mitochondrial function in renal cells

American journal of physiology. Renal physiology, 2006-10, Vol.291 (4), p.F840-F855

2006

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Protein kinase C-epsilon modulates mitochondrial function and active Na+ transport after oxidant injury in renal cells

American journal of physiology. Renal physiology, 2004-02, Vol.286 (2), p.F307-F316

2004

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Protein kinase C-belongs to modulates mitochondrial function and active Na+ transport after oxidant injury in renal cells

American journal of physiology. Renal physiology, 2004-02, Vol.55 (2), p.F307

2004

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Protein kinase C-∈ modulates mitochondrial function and active Na+ transport after oxidant injury in renal cells

American journal of physiology. Renal physiology, 2004, Vol.55 (2), p.F307-F316

2004

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Activation of ERK1/2 pathway mediates oxidant-induced decreases in mitochondrial function in renal cells

American journal of physiology. Renal physiology, 2006-10, Vol.291 (4), p.31

2006

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Protein kinase Cε targets respiratory chain and mitochondrial membrane potential but not F0F1‐ATPase in renal cells injured by oxidant

Protein kinase Cε targets respiratory chain and mitochondrial membrane potential but not F 0 F 1 -ATPase in renal cells injured by oxidant

Succinate ameliorates energy deficits and prevents dysfunction of complex I in injured renal proximal tubular cells

Deletion of protein kinase C-ε attenuates mitochondrial dysfunction and ameliorates ischemic renal injury

Protein kinase C-α activation promotes recovery of mitochondrial function and cell survival following oxidant injury in renal cells

Protein Kinase C-α Interaction with F0F1-ATPase Promotes F0F1-ATPase Activity and Reduces Energy Deficits in Injured Renal Cells

Deletion of protein kinase C-e attenuates mitochondrial dysfunction and ameliorates ischemic renal injury

Protein kinase C-[alpha] activation promotes recovery of mitochondrial function and cell survival following oxidant injury in renal cells

Protein kinase C-α activation promotes recovery of mitochondrial function and cell survival following oxidant injury in renal cells

Protein kinase C-epsilon activation induces mitochondrial dysfunction and fragmentation in renal proximal tubules

Assessment of Mitochondrial Functions and Cell Viability in Renal Cells Overexpressing Protein Kinase C Isozymes

γ-Tocotrienol protects against mitochondrial dysfunction and renal cell death

Protein kinase C-[epsilon] activation induces mitochondrial dysfunction and fragmentation in renal proximal tubules

Protein kinase C-ε activation induces mitochondrial dysfunction and fragmentation in renal proximal tubules

Assessment of mitochondrial functions and cell viability in renal cells overexpressing protein kinase C isozymes

The repair of Na+‐dependent glucose uptake following injury is regulated by PKC‐α and PKC‐ε

Activation of ERK1/2 pathway mediates oxidant-induced decreases in mitochondrial function in renal cells

Protein kinase C-epsilon modulates mitochondrial function and active Na+ transport after oxidant injury in renal cells

Protein kinase C-belongs to modulates mitochondrial function and active Na+ transport after oxidant injury in renal cells

Protein kinase C-∈ modulates mitochondrial function and active Na+ transport after oxidant injury in renal cells

Activation of ERK1/2 pathway mediates oxidant-induced decreases in mitochondrial function in renal cells

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