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HEK 293 Tet-On 3G

RRID:CVCL_V350

Organism

Homo sapiens

Comments

Characteristics: Transfected with reverse tetracycline-controlled transactivator (rtTA), a fusion between a mutated version of E.coli TetR and the activating domain of HSV-1 VP16. Transfected with: UniProtKB; P04483; E.coli Tn10 tetR. Transfected with: UniProtKB; P04486; Human herpesvirus 1 VP16 (UL28) (with del 1-360). Transformant: NCBI_TaxID; 28285; Adenovirus 5. DT Created: 16-04-14; Last updated: 07-09-18; Version: 7

Proper Citation

RRID:CVCL_V350

Category

Transformed cell line DT Created: 16-04-14; Last updated: 07-09-18; Version: 7

Sex

DT Created: 16-04-14; Last updated: 07-09-18; Version: 7

Synonyms

HEK293 Tet-On 3G DT Created: 16-04-14, Last updated: 07-09-18, Version: 7

Cross References

BTO; BTO:0003347 Wikidata; Q54882282 DT Created: 16-04-14; Last updated: 07-09-18; Version: 7

Hierarchy

DT Created: 16-04-14; Last updated: 07-09-18; Version: 7

Originate from Same Individual

DT Created: 16-04-14; Last updated: 07-09-18; Version: 7

Publications that use this research resource

Dual leucine zipper kinase-dependent PERK activation contributes to neuronal degeneration following insult.

  • Larhammar M
  • Elife
  • 2017 Apr 25

Literature context:


Abstract:

The PKR-like endoplasmic reticulum kinase (PERK) arm of the Integrated Stress Response (ISR) is implicated in neurodegenerative disease, although the regulators and consequences of PERK activation following neuronal injury are poorly understood. Here we show that PERK signaling is a component of the mouse MAP kinase neuronal stress response controlled by the Dual Leucine Zipper Kinase (DLK) and contributes to DLK-mediated neurodegeneration. We find that DLK-activating insults ranging from nerve injury to neurotrophin deprivation result in both c-Jun N-terminal Kinase (JNK) signaling and the PERK- and ISR-dependent upregulation of the Activating Transcription Factor 4 (ATF4). Disruption of PERK signaling delays neurodegeneration without reducing JNK signaling. Furthermore, DLK is both sufficient for PERK activation and necessary for engaging the ISR subsequent to JNK-mediated retrograde injury signaling. These findings identify DLK as a central regulator of not only JNK but also PERK stress signaling in neurons, with both pathways contributing to neurodegeneration.