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Validated All-in-One™ qPCR Primer for BTG2(NM_006763.2) Search again
Product ID:
HQP018780
(click here to view gene annotation page)
Species:
Human
Symbol:
Alias:
APRO1, PC3, TIS21
Gene Description:
BTG anti-proliferation factor 2
Target Gene Accession:
NM_006763.2(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
Summary
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. [provided by RefSeq].
Gene References into function
- PC3 / BTG2 inhibits the proliferation of different types of cells, including neural cells.
- First evidence that BTG2 is a target of p53 and is activated p53-dependently by DNA damage.
- First evidence showing that PC3 / BTG2 acts as cell cycle checkpoint at G1 phase by inhibiting the expression of cyclin D1
- This review describes BTG2 / PC3 as link between p53 and pRb. p53 via BTG2 / PC3 may activate pRb, since the BTG2 / PC3 product promotes accumulation of hypophosphorylated pRb by reducing cyclin D1 protein levels and thereby inhibiting CDK4 activity.
- Transient expression assays with BTG2/TIS21/PC3 promoter deletions and electrophoretic mobility shift analysis identified a major wild-type p53 response element located -74 to -122 relative to the start codon.
- Antiproliferative proteins of the BTG/Tob family are degraded by the ubiquitin-proteasome system. the C-terminal regions are necessary and sufficient to control the stabilities of BTG1, BTG2, Tob, and Tob2 proteins.
- BTG2 interacts with the CCR4 complex and has a role in cell-cycle regulation
- PC3 / BTG2 induces neural precursors to shift from proliferation to differentiation. This differentiative action occurs in cerebellar progenitors by a dual mechanism: inhibition of cell cycle (of cyclin D1) and induction of the proneural gene Math1.
- deregulation of BTG2 may be an important step in the development of mammary tumors
- DeltaNp73alpha not only acts as an inhibitor of p53/TAp73 functions in neuroblastoma tumors, but also cooperates with wt-p53 in playing a physiological role through the activation of BTG2TIS21/PC3 gene expression
- binding of tis21/BTG2/pc3 to Pin-1 or cyclin B1-Cdc2 complex and induction of mitochondrial depolarization are responsible for the antiproliferative effects of EGF in human tumor cells
- BTG2 expression was found to be significantly reduced in a large proportion of human kidney and breast carcinomas, suggesting that BTG2 is a tumor suppressor that links p53 and Rb pathways in human tumorigenesis.
- BTG2 contributes to retinoic acid activity by favoring differentiation through a gene-specific modification of histone H4 arginine methylation and acetylation levels.
- Reverse-transcription polymerase chain reaction confirmed increased expression of GADD45A, BTG2, PDE4B, and CEBPD and downregulation of TOB1 in skeletal muscle intradialysis.
- PC3 / BTG2 acts as a tumor suppressor of medulloblastoma by its antiproliferative and prodifferentiative effect on cerebellar progenitors. This antagonizes Shh and appears physiologic since endogenous PC3 / BTG2 decreases in human medulloblastomas.
- T3 upregulates proliferation of LNCaP cells by downregulating BTG2 gene expression through the consensus TRE pathway.
- BTG2 expression may play a role at a very early point during the differentiation processes of hematopoietic cells.
- BTG2 is a general activator of mRNA decay, thereby contributing to gene expression control.
- TIS21 negatively regulated hepatocarcinogenesis in part by disruption of the FoxM1-cyclin B1 regulatory loop, thereby inhibiting proliferation of transformed cells developed in mouse and human livers.
- BTG2/TIS21/PC3 enhances cancer cell death by accumulating H2O2 via imbalance of the antioxidant enzymes in response to chemotherapy.
- Crystal structure of human BTG2 reveal the putative CAF1 binding site.
- Estradiol downregulation of the tumor suppressor gene BTG2 requires estrogen receptor-alpha and the REA corepressor
