Disease relevance of ccnd1

• The resulting downregulation of cyclin D1 protein resulted in microophthalmia and microcephaly, but not lethality [1].

High impact information on ccnd1

• Antisense inhibition of cyclin D1 expression is equivalent to flavopiridol for radiosensitization of zebrafish embryos [2].
• Conclusions: Treatment of zebrafish embryos with flavopiridol enhanced radiation sensitivity of zebrafish embryos to a degree that was very similar to that associated with downregulation of cyclin D1 expression [2].
• This was particularly evident for the IR-induced curly up phenotype, which was greatly exacerbated by both flavopriridol and cyclin D1 downregulation [2].
• The effect of HDAC1 on cell cycle exit is cell-autonomous, and loss of HDAC1 in the retina leads to up-regulation of cyclin D and E transcripts [3].
• Coordinate control of cell cycle regulatory genes in zebrafish development tested by cyclin D1 knockdown with morpholino phosphorodiamidates and hydroxyprolyl-phosphono peptide nucleic acids [1].

Biological context of ccnd1

• The phenotypes were not seen with 3-mismatch MO 20mers or 1-mismatch HypNA-pPNA 16mers, and were rescued by an exogenous ccnd1 mRNA construct with five mismatches [1].
• Zebrafish cyclin D1 is differentially expressed during early embryogenesis [4].
• The initial expression of cyclin D1 transcript occurs at the presumed onset of G1 phase in the developing zebrafish embryo [4].
• We have isolated and determined the nucleotide sequence of a cDNA containing the complete coding region of cyclin D1 from embryonic zebrafish cDNA library [4].
• The cyclin D1 gene is a single copy gene within the zebrafish genome, which undergoes an alternative polyadenylation process [4].

Associations of ccnd1 with chemical compounds

• Cyclin D1-deficient embryos had virtually identical IR sensitivity profiles when compared with embryos treated with flavopiridol [2].

Analytical, diagnostic and therapeutic context of ccnd1

• To investigate the regulation of this process further, the translation of ccnd1 mRNA, a G1/S checkpoint control element, was impaired by microinjection of ccnd1-specific morpholino phosphorodiamidate (MO) 20mer or hydroxyprolyl-phosphono peptide nucleic acid (HypNA-pPNA) 16mer antisense oligonucleotides [1].

References