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Id Genes (id + gene)

Distribution by Scientific Domains

Medical Sciences	75%

Selected Abstracts

Non-redundant inhibitor of differentiation (Id) gene expression and function in human prostate epithelial cells

THE PROSTATE, Issue 9 2006
Ananthi J. Asirvatham
Abstract BACKGROUND The four Id (inhibitor of differentiation) proteins (Id1, Id2, Id3, and Id4) dimerize and neutralize the transcriptional activity of basic helix-loop-helix (bHLH) proteins. The Id proteins negatively regulate differentiation and promote proliferation hence the expression of specific subsets of Id proteins is high in many different types of cancers. However, the expression of all the Id isoforms and their potential function in specific cancer cell types is not known. In this study, the expression and function of all four Id isoforms in prostate cancer cell lines was investigated to gain a better understanding of the role of each Id isoform in normal prostate epithelial and prostate cancer cells. METHODS Id gene and protein expression was evaluated in the context of androgen response. The cellular function of Id isoforms was evaluated by targeted loss of function of Id genes. RESULTS The four Id isoforms are differentially expressed and regulated in normal human prostate epithelial cells versus prostate cancer cell lines DU145 and LNCaP. Id4 is present only in AR positive cells (normal and LNCaP) and its expression regulated by androgens. Loss of Id1 and Id3 expression by siRNA results in loss of proliferation. Loss of Id2 had no effect on proliferation but increased apoptosis. CONCLUSIONS A complex equilibrium between Id isoforms determines the cell fate. Id1 and Id3 target cellular proliferation, Id2 targets apoptosis, and Id4 may act as a potential tumor suppressor in prostate epithelial cells. Prostate 66: 921,935, 2006. © 2006 Wiley-Liss, Inc. [source]

Id1 expression is transcriptionally regulated in radial growth phase melanomas

INTERNATIONAL JOURNAL OF CANCER, Issue 8 2007
Byungwoo Ryu
Abstract Id genes have been demonstrated to be upregulated in a wide variety of human malignancies and their expression has been correlated with disease prognosis; however, little is known about the mechanisms of Id gene activation in tumors. We have previously shown that the helix-loop-helix transcription factor, Id1, is highly expressed in primary human melanomas during the radial growth phase and that Id1 is a transcriptional repressor of the familial melanoma gene CDKN2A. Here we use a series of melanoma cell lines that recapitulate the phenotypic characteristics of melanomas at varying stages of malignant progression to evaluate the expression levels of Id1 in this model system and determine the mechanism of Id1 dysregulation in these tumor cells. We find elevated protein levels of Id1 to be present consistently in radial growth phase tumor cells in accordance with our primary tumor data. Id1 transcript levels were also found to be elevated in these radial growth phase melanoma cells without any appreciable evidence of gene amplification and Id1 promoter activity was found to correlate with Id expression levels. We therefore conclude that Id1 expression is primarily regulated at the transcriptional level in radial growth phase melanomas and expect that therapies that target Id1 gene expression may be useful in the treatment of Id-associated malignancies. © 2007 Wiley-Liss, Inc. [source]

Inhibitory helix-loop-helix transcription factors Id1/Id3 promote bone formation in vivo

JOURNAL OF CELLULAR BIOCHEMISTRY, Issue 2 2004
Yukiko Maeda
Abstract Bone formation is under the control of a set of transcription factors. Ids are inhibitory helix-loop-helix (HLH) transcription factors and expression of Id genes in osteoblasts is under the control of calciotropic agents such as BMP and vitamin D. However, the function of Ids during bone formation in vivo has not yet been elucidated. We, therefore, examined the role of Id1 and Id3 in the regulation of bone metabolism in vivo. Using wild type and Id1/Id3 heterozygous knockout mice, we analyzed calvarial bone formation in the suture by X-ray picture, proliferation, and mineralization activities of primary calvarial osteoblasts by MTT assay and alizarin red staining and onthotopic in vivo bone formation by BMP injection onto calvaria and micro CT analysis. The width of calvarial sutures was reduced by more than 50% in Id1/Id3 heterozygous knock out mice. Analyses on the cellular basis for the mechanism underlying the defects in the mutant mice revealed suppression of proliferation and mineralization in osteoblasts derived from Id1/Id3 heterozygous knock out mice. Furthermore, Id1/Id3 heterozygous knock out mice suppressed BMP-induced bone formation in vivo. These results indicated that Id1 and Id3 are positive factors to promote bone formation in vivo. © 2004 Wiley-Liss, Inc. [source]