A Defect in Nurturing in Mice Lacking the Immediate Early Gene fosB

@article{Brown1996ADI,
  title={A Defect in Nurturing in Mice Lacking the Immediate Early Gene fosB},
  author={Jennifer R. Brown and Hong Ye and Roderick T Bronson and Pieter Dikkes and Michael Eldon Greenberg},
  journal={Cell},
  year={1996},
  volume={86},
  pages={297-309}
}

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References

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Bone and haematopoietic defects in mice lacking c-fos
TLDR
It is reported that heterozygous fos +/− mice appear normal, although females exhibit a distorted transmission frequency, which defines the c-Fos protein as an essential molecule for the development of specific cellular compartments.
Proto-oncogene FosB: the amino terminus encodes a regulatory function required for transformation.
TLDR
It is reported that transformation by FosB also requires an intact DNA-binding domain composed of the functionally bipartite basic region and leucine zipper as well as sequences present in the N terminus that serve a regulatory function.
Null Mutation of c-fos Impairs Structural and Functional Plasticities in the Kindling Model of Epilepsy
TLDR
The hypothesis that the null mutation of c-fos attenuates a pathological activity-determined functional plasticity (kindling development) as well as a structural Plasticity (mossy fiber reorganization) is supported.
Differential expression of immediate early genes after hippocampal long-term potentiation in awake rats.
The product of a novel growth factor activated gene, fos B, interacts with JUN proteins enhancing their DNA binding activity.
TLDR
Immunoprecipitation studies showed that fos B as c‐fos protein, forms a complex in vitro with c‐jun and jun B proteins in the absence of a target binding sequence, suggesting thatfos B protein plays a role in control of gene expression.
Alternative splicing of fosB transcripts results in differentially expressed mRNAs encoding functionally antagonistic proteins.
TLDR
It is shown that serum-stimulated fibroblasts transiently express two different forms of fosB mRNA, which are generated by alternative splicing of the transcript from a single gene, indicating a new mechanisms regulating the action of members of the Fos family.
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