Santa Cruz Biotechnology

Tom20 (F-10)

#sc-17764 · western blot

67

Evidence Score · Well-Established

Used by 94 independent labs across 202 papers. How we score this →

200

Citing papers

5.7k

Combined citations

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Research areas

Mitochondrial Function and Pathology33 Autophagy in Disease and Therapy25 ATP Synthase and ATPases Research13 Endoplasmic Reticulum Stress and Disease10 Cell death mechanisms and regulation9 RNA modifications and cancer9 interferon and immune responses8 Cancer, Hypoxia, and Metabolism7

Papers citing this product

1

Pathological structural conversion of α-synuclein at the mitochondria induces neuronal toxicity

Nature Neuroscience·2022·253 cit.·DOI

2

Reactive oxygen species trigger Parkin/PINK1 pathway–dependent mitophagy by inducing mitochondrial recruitment of Parkin

Journal of Biological Chemistry·2017·240 cit.·DOI

3

Cisplatin resistance involves a metabolic reprogramming through ROS and PGC-1α in NSCLC which can be overcome by OXPHOS inhibition

Free Radical Biology and Medicine·2019·215 cit.·DOI

4

Cardiolipin exposure on the outer mitochondrial membrane modulates α-synuclein

Nature Communications·2018·197 cit.·DOI

5

MCU encodes the pore conducting mitochondrial calcium currents

eLife·2013·183 cit.·DOI

6

Upregulation of Rubicon promotes autosis during myocardial ischemia/reperfusion injury

Journal of Clinical Investigation·2020·146 cit.·DOI

7

Optineurin-mediated mitophagy protects renal tubular epithelial cells against accelerated senescence in diabetic nephropathy

Cell Death and Disease·2018·144 cit.·DOI

8

Heterozygous PINK1 p.G411S increases risk of Parkinson’s disease via a dominant-negative mechanism

Brain·2016·142 cit.·DOI

9

Cancer-associated fibroblasts modify lung cancer metabolism involving ROS and TGF-β signaling

Free Radical Biology and Medicine·2018·140 cit.·DOI

10

Mitophagy protein PINK1 suppresses colon tumor growth by metabolic reprogramming via p53 activation and reducing acetyl-CoA production

Cell Death and Differentiation·2021·128 cit.·DOI

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