... We purchased the following antibodies: rabbit anti-BCL6 monoclonal antibody (EP529Y; Epitomics, Burlingame, CA, USA); rabbit anti-cyclin D2 polyclonal antibody (M-20: sc-593; Santa Cruz Biotechnology, Santa Cruz, CA, USA); ...
RT-qPCR was performed to determine the regulatory mechanism of Herp knockdown in the cell cycle, and in steroid synthesis, RT-qPCR analysis revealed that Herp knockdown upregulated the mRNA expression of steroidogenic enzymes (Cyp19a1) and downregulated metabolic enzymes (Cyp1b1) and cell cycle factors (cyclin A1, cyclin B1 and cyclin D2).
Shi et al., Nanning, China. In Theriogenology, Dec 2015
Adding BMP1 recombinant protein to the culture medium of the GCs increased the expression of the key cell cycle regulators such as cyclin D1 and cyclin D2 and downregulated the expression of cell apoptosis pathway genes such as Cytochrome C, Fas, FasL, and Chop, both at the mRNA and at the protein levels.
Sheridan et al., Seattle, United States. In Nat Genet, 2014
Here we report that individuals with MPPH lacking upstream PI3K-AKT pathway mutations carry de novo mutations in CCND2 (encoding cyclin D2) that are clustered around a residue that can be phosphorylated by glycogen synthase kinase 3β (GSK-3β).
Bydlowski et al., São Paulo, Brazil. In Anticancer Agents Med Chem, 2013
AZT down-regulated the pro-proliferative genes encoding AKT1, MYC, STAT1, MAPK8, MAPK9, CCL-3, Bcl-3, and cyclin D2; pro-angiogenenic genes encoding VEGF and IL8; and genes involved in cell adhesion (ICAM1 and FN1) and the NF-κB pathway.
Aifantis et al., New York City, United States. In Cancer Cell, 2012
Although cyclin D functions appear largely tissue specific, we demonstrate that cyclin D3 has unique functions in lymphocyte development and cannot be replaced by cyclin D2, which is also expressed during blood differentiation.
Ferrando et al., New York City, United States. In Nat Med, 2009
In contrast, glucocorticoid treatment induced transcriptional upregulation of cyclin D2 (Ccnd2) and protected mice from developing the intestinal goblet cell metaplasia typically induced by inhibition of NOTCH signaling with GSIs.