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CAMK4 — HDAC4

Pathways - manually collected, often from reviews:

• OpenBEL Selventa BEL large corpus: Complex of HDAC4-MEF2A → CAMK4 (decreases, HDAC4/MEF2A Activity)
  Evidence: Association of MEF2 with HDAC4/5 can also be inhibited by cotransfection with a constitutively active fragment of CaMKI/IV, which may provide an indirect mechanism for CaMKI/IV enhancement of MEF2 transcription (53).
• NCI Pathway Database Signaling events mediated by HDAC Class II: HDAC4 (HDAC4) → CaMK IV (CAMK4) (modification, collaborate) Davis et al., J Biol Chem 2003*
  Evidence: assay, physical interaction

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

• IRef Biogrid Interaction: HDAC4 — CAMK4 (direct interaction, enzymatic study) Zhao et al., J Biol Chem 2001*
• IRef Hprd Interaction: HDAC4 — CAMK4 (in vivo) Zhao et al., J Biol Chem 2001*
• IRef Hprd Interaction: HDAC4 — CAMK4 (in vitro) Zhao et al., J Biol Chem 2001*

Text-mined interactions from Literome

Bolger et al., J Neurosci 2005 : However, in response to low-potassium or excitotoxic glutamate conditions that induce neuronal cell death, HDAC4 rapidly translocates into the nucleus of cultured CGNs. Treatment with the neuronal survival factor BDNF suppresses HDAC4 nuclear translocation, whereas a proapoptotic CaMK inhibitor stimulates HDAC4 nuclear accumulation
Guan et al., Am J Physiol Cell Physiol 2012 : In addition, CaMKIV is required for HDAC4 phosphorylation, which is required for HDAC4 association with the cytoplasmic protein 14-3-3 ... Our results demonstrate that CaMKIV induces chondrocyte differentiation through regulation of HDAC4 subcellular relocation, from the nucleus to the cytoplasm, which results in increased activity of RunX2 and transition of chondrocytes from the proliferative to the prehypertrophic stage