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Rabbit Anti-PDK1, phospho (Ser241) Monoclonal Antibody, Unconjugated, Clone C49H2


Antibody ID


Target Antigen

Pdk1 human, mouse, rat

Proper Citation

(Cell Signaling Technology Cat# 3438, RRID:AB_2161134)


monoclonal antibody


Applications: W, IP. Consolidation on 10/2018: AB_10364803, AB_10366540, AB_2161134, AB_2299372.

Host Organism



Cell Signaling Technology

Cat Num


Publications that use this research resource

Inducible and reversible phenotypes in a novel mouse model of Friedreich's Ataxia.

  • Chandran V
  • Elife
  • 2017 Dec 19

Literature context:


Friedreich's ataxia (FRDA), the most common inherited ataxia, is caused by recessive mutations that reduce the levels of frataxin (FXN), a mitochondrial iron binding protein. We developed an inducible mouse model of Fxn deficiency that enabled us to control the onset and progression of disease phenotypes by the modulation of Fxn levels. Systemic knockdown of Fxn in adult mice led to multiple phenotypes paralleling those observed in human patients across multiple organ systems. By reversing knockdown after clinical features appear, we were able to determine to what extent observed phenotypes represent reversible cellular dysfunction. Remarkably, upon restoration of near wild-type FXN levels, we observed significant recovery of function, associated pathology and transcriptomic dysregulation even after substantial motor dysfunction and pathology were observed. This model will be of broad utility in therapeutic development and in refining our understanding of the relative contribution of reversible cellular dysfunction at different stages in disease.

Funding information:
  • NCRR NIH HHS - S10 RR019391(United States)

Loss of Frataxin activates the iron/sphingolipid/PDK1/Mef2 pathway in mammals.

  • Chen K
  • Elife
  • 2016 Nov 30

Literature context:


Friedreich's ataxia (FRDA) is an autosomal recessive neurodegenerative disease caused by mutations in Frataxin (FXN). Loss of FXN causes impaired mitochondrial function and iron homeostasis. An elevated production of reactive oxygen species (ROS) was previously proposed to contribute to the pathogenesis of FRDA. We recently showed that loss of frataxin homolog (fh), a Drosophila homolog of FXN, causes a ROS independent neurodegeneration in flies (Chen et al., 2016). In fh mutants, iron accumulation in the nervous system enhances the synthesis of sphingolipids, which in turn activates 3-phosphoinositide dependent protein kinase-1 (Pdk1) and myocyte enhancer factor-2 (Mef2) to trigger neurodegeneration of adult photoreceptors. Here, we show that loss of Fxn in the nervous system in mice also activates an iron/sphingolipid/PDK1/Mef2 pathway, indicating that the mechanism is evolutionarily conserved. Furthermore, sphingolipid levels and PDK1 activity are also increased in hearts of FRDA patients, suggesting that a similar pathway is affected in FRDA.

Funding information:
  • NIDDK NIH HHS - U24 DK059637(United States)