NCAM1Cell Adhesion Molecule, Neural, 1
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Similar to our results of 53% of the sample with NCAM1 gene expression, Rubinek et al.
The absence of SNA/2 overexpression and of CDH1 and NCAM1 suppression suggests that they are not associated with tumor invasiveness in GH-secreting pituitary adenomas.
CDH1 SNAI2 NCAM1 Gene expression (n=20) (n=12) (n=15) n (%) 10 (50%) 0 (0%) 8 (53.
We used transcript concentrations of marker genes GATA1, RUNX1, SPI1, and NCAM1, commonly involved in leukemogenesis, to study the need for stabilization of BM samples in a clinical setting of disease monitoring.
Q-RT-PCR was performed in a 1-step method with 1 ng total RNA by use of the Quantitect[R] SYBR[R] Green reverse-transcription (RT)-PCR Kit and Quantitect Primer Assays (Qiagen) for the detection of GATA1, RUNX1, NCAM1, and SPI1 and for control gene 18S rRNA.
We observed lower mean (SD) gene expression at P2 vs R2 for all genes: GATA1 70 (12)%, RUNX1 50 (11)%, NCAM1 41 (8)%, and SPI1 51 (6)%.
The genes to be analyzed were selected because of their attributes as key regulators during different stages of hematopoiesis and leukemogenesis, as well as their more or less distinct organ specificity: NCAM1 and RUNX1 as representatives of genes with functions (hematopoiesis, osteogenesis, cell adhesion) on many cell types (hematopoietic cells, neurons, muscles) of various differentiated tissues (embryonic cells, differentiated cells), GATA1 and SPI1 having more circumscribed compartments and cell types (erythropoiesis/megakaryopoiesis, myelopoiesis, and lymphopoiesis).