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Peroxisome proliferator-activated receptor alpha (PPARalpha) target gene expression was almost absent in contrast to increased lipid synthesis in the TIS21 protein (TIS21) knockout (TIS21-KO) mice compared to WT mice.
Tumor suppressors BTG1 and BTG2 regulate early mouse B-cell development.
Results identify a key molecular mechanism by which the BTG2-PRMT1 module regulates pre-B cell differentiation and inhibits pre-B cell leukemogenesis.
Results suggest that Btg2 is an anti-adipogenic factor and its expression is controlled by the Stat3 signaling pathway.
these data show that both Btg1 and Btg2 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.
Btg2 overexpression in vivo and in vitro induced all the observed changes during interdigit regression, including oxidative stress, arrest of cell cycle progression, transcriptional regulation of senescence markers, and caspase-mediated apoptosis.
study provides a novel molecular mechanism of BTG2-mediated induction of hepcidin gene expression, thereby contributing to a better understanding of the hepatic hepcidin production involved in iron homeostasis
TIS21 is required for development of spiral ganglion cells
we show that the putative tumor suppressor gene Btg2 is consistently downregulated in high grade gliomas and that its downregulation is necessary for a cell to maintain the malignant phenotype.
Mice lacking the Tis21 3' UTR develop a microcephalic neocortex with fewer neurons.
BTG2 regulates hepatic glucose homeostasis via induction of orphan nuclear receptor Nur77 in diabetic mouse model.
pro-apoptotic pathway of CRP-CD32-Nox2-p53-BTG2 may contribute to the retardation of the atherogenic process
B-cell translocation gene 2 (BTG2) is a crucial regulator in GLP-1-induced insulin gene expression and insulin secretion via upregulation of pancreatic duodenal homeobox-1 (PDX-1) in pancreatic beta-cells.
The present study suggests a functional coupling between the GABAergic system and the transcriptional regulation of the two genes (Btg2 and Adamsts1) in the hippocampus of adult mice.
Tis21 induces migration of cerebellar granule neuron precursor cells through Cxcl3, which may represent a novel target for medulloblastoma therapy
These results identify PC3/Tis21 as a gene required in the control of proliferation and terminal differentiation of newborn neurons during adult hippocampal neurogenesis and suggest its involvement in the formation of contextual memories.
TIS21 has a role in the differentiation of osteoclasts
Cell cycle exit of cerebellar granule cell precursors and the onset of cerebellar neurogenesis are coordinated by PC3 through transcriptional control of cyclin D1 and Math1, respectively
TPA-induced TIS21 mRNA expression is mediated by PKC-delta, and TIS21 induces G2/M arrest and cell death by inhibiting cyclin B1-Cdc2 binding and the kinase activity through its binding to Cdc2.
btg2 regulates vertebral patterning by modulating bone morphogenetic protein/smad signaling
oncogenic miR-25-3p directly targets BTG2 in TNBC. Further studies revealed that the biological effects of miR-25-3p on TNBC cell proliferation and apoptosis were mediated through regulation of BTG2 and subsequent activation of AKT and ERK-MAPK signaling pathway.
Open data and immunohistochemical analysis were performed to confirm the role of TIS21(/BTG2) expression in various human breast cancer tissues. It was observed that TIS21(/BTG2) inhibited mTORc1 activity by reducing Raptor-mTOR interaction along with upregulation of tsc1 expression.
we found that miR-27-3p was overexpressed in gastric cancer tissues and cell lines and that BTG2 was a direct and functional target of miR-27a-3p in gastric cancer
decreases tumorigenesis of hepatocellular carcinoma cell line side population cells
Effect of TIS21 on the regulation of p53 activity was confirmed by knockdown of TIS21 expression by RNA interference.
TIS21 attenuated Doxorubicin-induced cancer cell senescence by inhibiting linear actin nucleation via Nox4-ROS-ABI2-DRF signal cascade
Data indicate that BTG2, MAP3K11, RPS6KA1 and PRDM1 as putative targets of microRNA miR-125b.
The results indicated that BTG2 expression was downregulated in skin cancer cell lines. Overexpression of BTG2 significantly inhibited cell proliferation, cell cycle progression, and the invasion and migration of skin cancer cells.
Overexpression of BTG2 inhibited the proliferation and migration/invasion of human osteosarcoma cells in vitro
clinical data support conclusions generated from patient-derived xenograft models and indicate that BTG2 expression is a candidate prognostic biomarker for TNBC.
miR-21 was found to be overexpressed and BTG2 was found to to be downregulated in HepG2 liver cancer cells.
BTG2 stimulates mRNA deadenylation via CAF1 activation through interaction with PABPC1. Interaction of BTG2 with the first RRM domain of PABPC1 is required for BTG2 to control cell proliferation.
SETD1A suppresses BTG2 expression through its induction of several BTG2-targeting miRNAs.
Results indicate that miR27a and BTG2 promote the migration and the growth of glioblastoma (GBM) cells and miR27a directly targets BTG2 in GBM cells.
Our results indicated that cisplatin attenuates prostate cancer cell proliferation partly mediated by upregulation of BTG2 through the p53-dependent pathway or p53-independent NFkappaB pathway.
In this review, we summarize the latest findings in BTG2 studies, highlighting the mechanisms for the regulatory effects of microRNAs (miRNAs) on BTG2 gene expression in the most common human cancers.
By applying loss-and-gain function analysis in NSCLC cell lines, we demonstrated that miR-25-BTG2 axis could directly regulated BTG2 expression and affect radiotherapy sensitivity of NSCLC cells.
An association with Graves disease was shown for several SNPs in BTG2.
BTG2 expression was inversely correlated with increased expression of the DNA methyltransferases DNMT1 and DNMT3a in MIBC, but not NMIBC, suggesting a potential role for BTG2 expression in muscle invasion of bladder cancer
Reactive oxygen spieces regulate Btg2/TIS21/PC3 expression via Protein kinase C-NFkappaappaB pathway.
The full length sequences of cDNA and genomic DNA of BTG2 gene from the porcine skeletal muscle, was cloned.
The protein encoded by this gene is a member of the BTG/Tob family. This family has structurally related proteins that appear to have antiproliferative properties. This encoded protein is involved in the regulation of the G1/S transition of the cell cycle.
B-cell translocation gene 2, anti-proliferative
, BTG family, member 2
, protein BTG2
, B-cell translocation gene 2
, B cell translocation protein 2
, BTG family member 2
, NGF-inducible protein TIS21
, NGF-inducible anti-proliferative protein PC3
, nerve growth factor-inducible anti-proliferative
, pheochromacytoma cell-3
, B-cell translocation protein 2
, Early induced gene B-cell translocation gene 2
, NGF-inducible anti-proliferative putative secreted protein
, cell surface alloantigen