Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UNIPROT:P50502 (
Hip
)
7,003
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Dyslexia, or specific reading disability, is the unexpected failure in learning to read and write when intelligence and senses are normal. One of the susceptibility genes,
DYX1C1
, has been implicated in neuronal migration, but little is known about its interactions and functions. As
DYX1C1
was suggested to interact with the U-box protein CHIP (carboxy terminus of
Hsc70-interacting protein
), which also participates in the degradation of estrogen receptors alpha (ERalpha) and beta (ERbeta), we hypothesized that the effects of
DYX1C1
might be at least in part mediated through the regulation of ERs. ERs have shown to be important in brain development and cognitive functions. Indeed, we show that
DYX1C1
interacts with both ERs in the presence of 17beta-estradiol, as determined by co-localization, co-immunoprecipitation and proximity ligation assays. Protein levels of endogenous ERalpha or exogenous ERbeta were reduced upon over-expression of
DYX1C1
, resulting in decreased transcriptional responses to 17beta-estradiol. Furthermore, we detected in vivo complexes of
DYX1C1
with ERalpha or ERbeta at endogenous levels along neurites of primary rat hippocampal neurons. Taken together, our data suggest that
DYX1C1
is involved in the regulation of ERalpha and ERbeta, and may thus affect the brain development and regulate cognitive functions. These findings provide novel insights into the function of
DYX1C1
and link neuronal migration and developmental dyslexia to the estrogen-signaling effects in the brain.
...
PMID:Functional interaction of DYX1C1 with estrogen receptors suggests involvement of hormonal pathways in dyslexia. 1942 54
