Dr. Peter Fink Johnson D.M.D.
Prosthodontist | Prosthodontics
5565 Grossmont Center Dr Suite 1-110 La Mesa CA, 91942About
Dr. Peter Johnson is a prosthodontist practicing in La Mesa, CA. Dr. Johnson specializes in the restoration and replacement of teeth. Prosthodontists maintain oral function, comfort and the appearance and health either with the natural teeth or the replacement of missing ones with maxillofacial tissues and artificial substances.
Provider Details
Expert Publications
Data provided by the National Library of Medicine- CCAAT/enhancer binding protein-beta is a mediator of keratinocyte survival and skin tumorigenesis involving oncogenic Ras signaling.
- Regulation of CCAAT/enhancer-binding protein (C/EBP) activator proteins by heterodimerization with C/EBPgamma (Ig/EBP).
- MEKK1 plays a critical role in activating the transcription factor C/EBP-beta-dependent gene expression in response to IFN-gamma.
- Transcriptional activity of CCAAT/enhancer-binding proteins is controlled by a conserved inhibitory domain that is a target for sumoylation.
- An essential role for a MEK-C/EBP pathway during growth factor-regulated cortical neurogenesis.
- Structural basis for DNA recognition by the basic region leucine zipper transcription factor CCAAT/enhancer-binding protein alpha.
- Nulliparous CCAAT/enhancer binding proteindelta (C/EBPdelta) knockout mice exhibit mammary gland ductal hyperlasia.
- Treatment considerations of fixed prosthetic restorations of the compromised
- Critical prosurvival roles for C/EBP beta and insulin-like growth factor I in macrophage tumor cells.
- Synergistic effect of dexamethasone and beta-adrenergic receptor agonists on the nerve growth factor gene transcription.
- Cell cycle-dependent phosphorylation of C/EBPbeta mediates oncogenic cooperativity between C/EBPbeta and H-RasV12.
- BCL-3 and NF-kappaB p50 attenuate lipopolysaccharide-induced inflammatory responses in macrophages.
- Repression of the inhibin alpha-subunit gene by the transcription factor CCAAT/enhancer-binding protein-beta.
- A role for mixed lineage kinases in regulating transcription factor CCAAT/enhancer-binding protein-{beta}-dependent gene expression in response to interferon-{gamma}.
- Molecular stop signs: regulation of cell-cycle arrest by C/EBP transcription factors.
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