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Vinculin antibody [EPR8185]


Antibody ID


Target Antigen

Vinculin antibody [EPR8185] rat, human, mouse, rat

Proper Citation

(Abcam Cat# ab129002, RRID:AB_11144129)


monoclonal antibody


validation status unknown, seller recommendations provided in 2012: Western Blot; Immunocytochemistry; Immunoprecipitation; Immunofluorescence; ICC/IF, IP, WB

Host Organism




Cat Num


Publications that use this research resource

Basal Mitophagy Occurs Independently of PINK1 in Mouse Tissues of High Metabolic Demand.

  • McWilliams TG
  • Cell Metab.
  • 2018 Feb 6

Literature context:


Dysregulated mitophagy has been linked to Parkinson's disease (PD) due to the role of PTEN-induced kinase 1 (PINK1) in mediating depolarization-induced mitophagy in vitro. Elegant mouse reporters have revealed the pervasive nature of basal mitophagy in vivo, yet the role of PINK1 and tissue metabolic context remains unknown. Using mito-QC, we investigated the contribution of PINK1 to mitophagy in metabolically active tissues. We observed a high degree of mitophagy in neural cells, including PD-relevant mesencephalic dopaminergic neurons and microglia. In all tissues apart from pancreatic islets, loss of Pink1 did not influence basal mitophagy, despite disrupting depolarization-induced Parkin activation. Our findings provide the first in vivo evidence that PINK1 is detectable at basal levels and that basal mammalian mitophagy occurs independently of PINK1. This suggests multiple, yet-to-be-discovered pathways orchestrating mammalian mitochondrial integrity in a context-dependent fashion, and this has profound implications for our molecular understanding of vertebrate mitophagy.

Funding information:
  • NHLBI NIH HHS - R01 HL074894(United States)

Type 2 Diabetes Variants Disrupt Function of SLC16A11 through Two Distinct Mechanisms.

  • Rusu V
  • Cell
  • 2017 Jun 29

Literature context:


Type 2 diabetes (T2D) affects Latinos at twice the rate seen in populations of European descent. We recently identified a risk haplotype spanning SLC16A11 that explains ∼20% of the increased T2D prevalence in Mexico. Here, through genetic fine-mapping, we define a set of tightly linked variants likely to contain the causal allele(s). We show that variants on the T2D-associated haplotype have two distinct effects: (1) decreasing SLC16A11 expression in liver and (2) disrupting a key interaction with basigin, thereby reducing cell-surface localization. Both independent mechanisms reduce SLC16A11 function and suggest SLC16A11 is the causal gene at this locus. To gain insight into how SLC16A11 disruption impacts T2D risk, we demonstrate that SLC16A11 is a proton-coupled monocarboxylate transporter and that genetic perturbation of SLC16A11 induces changes in fatty acid and lipid metabolism that are associated with increased T2D risk. Our findings suggest that increasing SLC16A11 function could be therapeutically beneficial for T2D. VIDEO ABSTRACT.

Funding information:
  • NHGRI NIH HHS - UM1 HG008895()
  • NIDDK NIH HHS - R01 DK066358()