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The protein Id: A negative regulator of helix-loop-helix DNA binding proteins
TLDR
It is proposed that HLH proteins lacking a basic region may negatively regulate other HLHprotein through the formation of nonfunctional heterodimeric complexes. Expand
Id1 and Id3 are required for neurogenesis, angiogenesis and vascularization of tumour xenografts
TLDR
Targeted disruption of the dominant negative helix–loop–helix proteins Id1 and Id3 in mice results in premature withdrawal of neuroblasts from the cell cycle and expression of neural-specific differentiation markers, which are required to maintain the timing of neuronal differentiation in the embryo and invasiveness of the vasculature. Expand
Impaired recruitment of bone-marrow–derived endothelial and hematopoietic precursor cells blocks tumor angiogenesis and growth
TLDR
It is demonstrated that recruitment of VEGF-responsive BM-derived precursors is necessary and sufficient for tumor angiogenesis and suggested new clinical strategies to block tumor growth are suggested. Expand
Identification of a Human Mitotic Checkpoint Gene: hsMAD2
TLDR
Human homolog of MAD2 was isolated and shown to be a necessary component of the mitotic checkpoint in HeLa cells by antibody electroporation experiments, suggesting that MAD2 might monitor the completeness of the spindle-kinetochore attachment. Expand
MAD2 haplo-insufficiency causes premature anaphase and chromosome instability in mammalian cells
TLDR
It is reported that deletion of one MAD2 allele results in a defective mitotic checkpoint in both human cancer cells and murine primary embryonic fibroblasts and Mad2+/- mice develop lung tumours at high rates after long latencies, implicating defects in the mitotic checkpoints in tumorigenesis. Expand
Mad2 overexpression promotes aneuploidy and tumorigenesis in mice.
TLDR
It is shown that overexpression of Mad2 in transgenic mice leads to a wide variety of neoplasias, appearance of broken chromosomes, anaphase bridges, and whole-chromosome losses, as well as acceleration of myc-induced lymphomagenesis. Expand
The myoD gene family: nodal point during specification of the muscle cell lineage.
TLDR
The myoD gene converts many differentiated cell types into muscle, and the helix-loop-helix motif is responsible for dimerization, and, depending on itsDimerization partner, MyoD activity can be controlled. Expand
Id proteins in development, cell cycle and cancer.
TLDR
The Id proteins have become important molecules for understanding basic biological processes as well as targets for potential therapeutic intervention in human disease. Expand
Rb inactivation promotes genomic instability by uncoupling cell cycle progression from mitotic control
TLDR
It is demonstrated how chromosome instability can arise as a by-product of defects in cell cycle control that compromise the accuracy of mitosis, and a new model is suggested to explain the frequent appearance of aneuploidy in human cancer. Expand
Overexpression of Id protein inhibits the muscle differentiation program: in vivo association of Id with E2A proteins.
TLDR
Evidence is presented that a model in which Id can inhibit muscle cell differentiation by associating with E proteins and preventing them from forming active hetero-oligomeric complexes with the muscle determination gene products is feasible. Expand
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