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Subventricular zone stem cells are endowed with a hidden supply of self-renewal capacity, coupled to cell cycle acceleration and emerging after ablation of the quiescence-maintaining Btg1 gene and following exercise.
Tumor suppressors BTG1 and BTG2 (zeige BTG2 Proteine) regulate early mouse B-cell development.
BTG1 has a role in regulating hepatic lipid metabolism and in preventing ATF4 (zeige ATF4 Proteine) and SCD1 (zeige SCD Proteine) from inducing liver steatosis
our results identify BTG1 as a tumor suppressor in leukemia that, when deleted, strongly enhances the risk of relapse in IKZF1-deleted B-cell precursor acute lymphoblastic leukemia, and augments the glucocorticoid resistance phenotype mediated by the loss of IKZF1 function.
Btg1 gain- and loss-of-function experiments were consistent with the pattern of expression of this gene in the developing digits. We detected a negative influence of BTG1 in the progress of cartilage maturation and a positive influence in the formation of fibrogenic tissue.
BTG1 overexpression or knockdown improved or impaired insulin (zeige INS Proteine) signaling respectively.
Btg1 regulates the proliferation of cerebellar granule precursors selectively through cyclin D1 (zeige CCND1 Proteine).
these data show that both Btg1 and Btg2 (zeige BTG2 Proteine) are required for normal vertebral patterning of the axial skeleton, but each gene contributes differently in specifying the identity along the anterior-posterior axis of the skeleton.
Antiproliferative BTG1 may participate in the activation-induced cell death of microglia by lowering the threshold for apoptosis.
BTG1 expression is lowered in colorectal cancer cells. Forced BTG1 expression reverses aggressive phenotypes in colorectal cancers.
BTG1 down-regulation in colorectal cancer occurs through epigenetic repression, which is involved in the development and progression of colorectal cancer.
BTG1 gene deletion is associated with acute lymphoblastic leukemia.
BTG1 interacts with ATF4 (zeige ATF4 Proteine) and positively modulates its activity by recruiting the protein arginine methyl transferase PRMT1 (zeige PRMT1 Proteine) to methylate ATF4 (zeige ATF4 Proteine) on arginine residue 239.
our data suggest that BTG1 overexpression combined with radiation therapy increases the therapeutic efficacy of breast cancer treatment via regulation of the cell cycle and apoptosis-related signaling pathways.
Suggest that down-regulated BTG1 expression might promote gastric carcinogenesis partially due to its promoter methylation. BTG1 overexpression might reverse the aggressive phenotypes.
Reduced BTG1 expression is associated with increased nasopharyngeal cancer severity, suggesting it is a negative regulator of the cancer and can serve as a prognostic indicator. Reduced BTG1 expression is possibly associated with tumour metastasis.
Our results indicate that altered BTG1 expression might affect hepatocarcinogenesis and may represent a novel biomarker for HCC (zeige FAM126A Proteine) carcinogenesis and progression.
Data indicate that microRNA-19a regulates prostate cancer cells by directly targeting B cell translocation gene-1 protein BTG1.
BTG1 may play an important role in the process of angiogenesis
This gene is a member of an anti-proliferative gene family that regulates cell growth and differentiation. Expression of this gene is highest in the G0/G1 phases of the cell cycle and downregulated when cells progressed through G1. The encoded protein interacts with several nuclear receptors, and functions as a coactivator of cell differentiation. This locus has been shown to be involved in a t(8\;12)(q24\;q22) chromosomal translocation in a case of B-cell chronic lymphocytic leukemia.
, BTG1 protein
, protein BTG1-like
, B-cell translocation gene 1 protein
, B-cell translocation gene 1, anti-proliferative
, anti-proliferative factor
, myocardial vascular inhibition factor
, B-cell translocation protein 1