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PINK1 Antibody


Antibody ID


Target Antigen

PINK1 species reactivity with these antibodies has not been determined cat bc 100-494 - the immunogen used for this antibody production has 100 homology with human protein, human

Proper Citation

(Novus Cat# BC100-494, RRID:AB_10127658)




validation status unknown, reseller suggested use: Immunofluorescence; ELISA; Western Blot; Immunocytochemistry; Immunocytochemistry, Immunofluorescence, Peptide ELISA, Western Blot

Host Organism




Cat Num


Publications that use this research resource

Neuronal Preconditioning Requires the Mitophagic Activity of C-terminus of HSC70-Interacting Protein.

  • Lizama BN
  • J. Neurosci.
  • 2018 Jun 22

Literature context:


C-terminus of HSC70-interacting protein (CHIP, STUB1) is a ubiquitously expressed cytosolic E3-ubiquitin ligase. CHIP-deficient mice exhibit cardiovascular stress and motor dysfunction prior to premature death. This phenotype is more consistent with animal models in which master regulators of autophagy are affected rather than with the mild phenotype of classic E3-ubiquitin ligase mutants. The cellular and biochemical events that contribute to neurodegeneration and premature aging in CHIP KO models remain poorly understood. Electron and fluorescent microscopy demonstrates that CHIP deficiency is associated with greater numbers of mitochondria, but these organelles are swollen and misshapen. Acute bioenergetic stress triggers CHIP induction and re-localization to mitochondria where it plays a role in the removal of damaged organelles. This mitochondrial clearance is required for protection following low-level bioenergetic stress in neurons. CHIP expression overlaps with stabilization of the redox stress sensor PTEN-inducible kinase 1 (PINK1) and is associated with increased LC3-mediated mitophagy. Introducing human promoter-driven vectors with mutations in either the E3 ligase or TPR domains of CHIP in primary neurons derived from CHIP-null animals enhances CHIP accumulation at mitochondria. Exposure to autophagy inhibitors suggests the increase in mitochondrial CHIP is likely due to diminished clearance of these CHIP-tagged organelles. Proteomic analysis of WT and CHIP KO mouse brains (4 male, 4 female per genotype) reveals proteins essential for maintaining energetic, redox and mitochondrial homeostasis undergo significant genotype-dependent expression changes. Together these data support the use of CHIP deficient animals as a predictive model of age-related degeneration with selective neuronal proteotoxicity and mitochondrial failure.Significance Statement: Mitochondria are recognized as central determinants of neuronal function and survival. We demonstrate that C-terminus of HSC70-Interacting Protein (CHIP) is critical for neuronal responses to stress. CHIP upregulation and localization to mitochondria is required for mitochondrial autophagy (mitophagy). Unlike other disease-associated E3 ligases such as Parkin and Mahogunin, CHIP controls homeostatic and stress-induced removal of mitochondria. While CHIP deletion results in greater numbers of mitochondria, these organelles have distorted inner membranes without clear cristae. Neuronal cultures derived from animals lacking CHIP are more vulnerable to acute injuries, and transient loss of CHIP renders neurons incapable of mounting a protective response following low-level stress. Together these data suggest that CHIP is an essential regulator of mitochondrial number, cell signaling and survival.

Funding information:
  • NCI NIH HHS - P50 CA128613(United States)
  • NIA NIH HHS - R01 AG033082()
  • NIEHS NIH HHS - R01 ES022936()

Male Brown Fat-Specific Double Knockout of IGFIR/IR: Atrophy, Mitochondrial Fission Failure, Impaired Thermogenesis, and Obesity.

  • Viana-Huete V
  • Endocrinology
  • 2018 Jan 1

Literature context:


It is unknown how the lack of insulin receptor (IR)/insulinlike growth factor I receptor (IGFIR) in a tissue-specific manner affects brown fat development and mitochondrial integrity and function, as well as its effect on the redistribution of the adipose organ and the metabolic status. To address this important issue, we developed IR/IGFIR double-knockout (DKO) in a brown adipose tissue-specific manner. Lack of those receptors caused severe brown fat atrophy, enhanced beige cell clusters in inguinal fat; loss of mitochondrial mass; mitochondrial damage related to cristae disruption; and the loss of proteins involved in autophagosome formation, mitophagy, mitochondrial quality control, and dynamics and thermogenesis. More important, DKO mice showed an impaired thermogenesis upon cold exposure, based on a failure in the mitochondrial fission mechanisms and a much lower uncoupling protein 1 transcription rate and content. As a result, DKO mice under normal conditions showed an obesity susceptibility, revealed by increased body fat mass and insulin resistance. Upon consumption of a high-fat diet, DKO mice displayed frank obesity, as shown by increased body weight, increased adiposity, insulin resistance, hyperinsulinemia, and hypertriglyceridemia, all consistent with a metabolic syndrome. Collectively, our data suggest a cause-and-effect relationship between failure in brown fat thermogenesis and increased adiposity and obesity.

Funding information:
  • NIDDK NIH HHS - P30 DK036836()
  • NIDDK NIH HHS - R01 DK031036()