Ca2+ Influx Regulates BDNF Transcription by a CREB Family Transcription Factor-Dependent Mechanism

@article{Tao1998Ca2IR,
  title={Ca2+ Influx Regulates BDNF Transcription by a CREB Family Transcription Factor-Dependent Mechanism},
  author={Xu Tao and Steven Finkbeiner and Donald B. Arnold and Adam J. Shaywitz and Michael Eldon Greenberg},
  journal={Neuron},
  year={1998},
  volume={20},
  pages={709-726}
}

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References

SHOWING 1-10 OF 188 REFERENCES
Calcium Influx via the NMDA Receptor Induces Immediate Early Gene Transcription by a MAP Kinase/ERK-Dependent Mechanism
TLDR
It is demonstrated that the transcription factors serum response factor (SRF) and Elk-1 can mediate glutamate induction of transcription through the SRE in cortical neurons, suggesting that SRF, Elk, and ERKs may have important roles in neuroplasticity.
L-type Voltage-sensitive Ca2+ Channel Activation Regulates c-fos Transcription at Multiple Levels (*)
TLDR
The results suggest that the phosphorylation and dephosphorylation of CREB controls its ability to regulate transcription in membrane-depolarized cells and that multiple pathways contribute to Ca2+-activated gene expression.
A Dominant-Negative Inhibitor of CREB Reveals that It Is a General Mediator of Stimulus-Dependent Transcription of c-fos
TLDR
The results suggest that CREB or its closely related family members are general mediators of stimulus-dependent transcription of c-fos and are required for at least some of the long-term actions of NGF.
Calcium/calmodulin-dependent protein kinase types II and IV differentially regulate CREB-dependent gene expression.
TLDR
The results demonstrate that CaMKIV, which is expressed in neuronal, reproductive, and lymphoid tissues, may act as a mediator of Ca(2+)-dependent gene induction.
CREB: a Ca(2+)-regulated transcription factor phosphorylated by calmodulin-dependent kinases.
TLDR
The results suggest that CaM kinases may transduce electrical signals to the nucleus and that CREB functions to integrate Ca2+ and cAMP signals.
Coupling of the RAS-MAPK Pathway to Gene Activation by RSK2, a Growth Factor-Regulated CREB Kinase
TLDR
Findings identify a cellular function for RSK2 and define a mechanism whereby growth factor signals mediated by RAS and MAPK are transmitted to the nucleus to activate gene expression.
...
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