GABPB2 antibody - C-terminal region (P100925_P050)
- Known as:
- GABPB2 (anti-) - C-terminal region (P100925_P050)
- Catalog number:
- p100925_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- GABPB2 antibody - C-terminal region (P100925_P050)
Related genes to: GABPB2 antibody - C-terminal region (P100925_P050)
- Gene:
- GABPB1 NIH gene
- Name:
- GA binding protein transcription factor subunit beta 1
- Previous symbol:
- GABPB2
- Synonyms:
- E4TF1-47, GABPB
- Chromosome:
- 15q21.2
- Locus Type:
- gene with protein product
- Date approved:
- 1994-01-18
- Date modifiied:
- 2018-04-23
- Gene:
- GABPB2 NIH gene
- Name:
- GA binding protein transcription factor subunit beta 2
- Previous symbol:
- -
- Synonyms:
- MGC29891
- Chromosome:
- 1q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 2008-02-25
- Date modifiied:
- 2018-04-23
Related products to: GABPB2 antibody - C-terminal region (P100925_P050)
Related articles to: GABPB2 antibody - C-terminal region (P100925_P050)
- Enhanced expression of TERT in gliomas is a result of two hotspot mutations, C228T and C250T, at the promoter region. GA-binding proteins selectively bind at these positions, respectively, causing an activation of the promoter and overexpression of TERT. GABP is a multimeric protein consisting of GABPA and GABPB with its isoforms GABPB1, GABPB1-L, GABPB1-S, GABPB2. In this study, we investigated the mRNA expression and association between TERT and GABPA/B isoforms in tumor samples of different glioma grades. The expression was determined by quantitative real-time PCR and the results were statistically analyzed. We present that TERT is mainly expressed in primary glioblastomas. All GA-binding proteins progress through the glioma grades and have the highest expression levels in secondary glioblastomas. In secondary glioblastomas after chemotherapy, GABPB1 and GABPB1-L are expressed on a lower level than without treatment. In high grades, TERT and GABPA, GAPB1, GABPB1-L, GABPB1-S are upregulated compared to low grades. Between primary and secondary glioblastomas with and without chemotherapy, TERT is elevated in the former while GABPB1 is increased in the secondary glioblastomas. GABPA and GABPB1, GABPB1-L and GABPB1-S positive correlate in primary glioblastomas. The present study confirms the upregulation of TERT in primary glioblastomas while all GABP proteins rise with the malignancy of the gliomas. Further investigations must be made to elucidate the relation between TERT and all GABP proteins as it may play a key role in the gliomagenesis. - Source: PubMed
Publication date: 2021/06/22
Papazacharias EfthymiosKuhl SaskiaRöhn GabrieleGörtz LukasGoldbrunner RolandTimmer Marco - Most glioblastomas (GBMs) achieve cellular immortality by acquiring a mutation in the telomerase reverse transcriptase () promoter. promoter mutations create a binding site for a GA binding protein (GABP) transcription factor complex, whose assembly at the promoter is associated with reactivation and telomere maintenance. Here, we demonstrate increased binding of a specific GABPB1L-isoform-containing complex to the mutant promoter. Furthermore, we find that promoter mutant GBM cells, unlike wild-type cells, exhibit a critical near-term dependence on GABPB1L for proliferation, notably also posttumor establishment in vivo. Up-regulation of the protein paralogue GABPB2, which is normally expressed at very low levels, can rescue this dependence. More importantly, when combined with frontline temozolomide (TMZ) chemotherapy, inducible GABPB1L knockdown and the associated reduction led to an impaired DNA damage response that resulted in profoundly reduced growth of intracranial GBM tumors. Together, these findings provide insights into the mechanism of cancer-specific regulation, uncover rapid effects of GABPB1L-mediated suppression in GBM maintenance, and establish GABPB1L inhibition in combination with chemotherapy as a therapeutic strategy for promoter mutant GBM. - Source: PubMed
Amen Alexandra MFellmann ChristofSoczek Katarzyna MRen Shawn MLew Rachel JKnott Gavin JPark Jesslyn EMcKinney Andrew MMancini AndrewDoudna Jennifer ACostello Joseph F - Hematopoietic stem cells (HSCs) and leukemic stem cells (LSCs) are both capable of self-renewal, with HSCs sustaining multiple blood lineage differentiation and LSCs indefinitely propagating leukemia. The GABP complex, consisting of DNA binding GABPα subunit and transactivation GABPβ subunit, critically regulates HSC multipotency and self-renewal via controlling an essential gene regulatory module. Two GABPβ isoforms, GABPβ1L and GABPβ2, contribute to assembly of GABPα(2)β(2) tetramer. We demonstrate that GABPβ1L/β2 deficiency specifically impairs HSC quiescence and survival, with little impact on cell cycle or apoptosis in differentiated blood cells. The HSC-specific effect is mechanistically ascribed to perturbed integrity of the GABP-controlled gene regulatory module in HSCs. Targeting GABPβ1L/β2 also impairs LSC self-renewal in p210(BCR-ABL)-induced chronic myelogenous leukemia (CML) and exhibits synergistic effects with tyrosine kinase inhibitor imatinib therapy in inhibiting CML propagation. These findings identify the tetramer-forming GABPβ isoforms as specific HSC regulators and potential therapeutic targets in treating LSC-based hematological malignancy. - Source: PubMed
Yu ShuyangJing XuefangColgan John DZhao Dong-MeiXue Hai-Hui - Neurons are unique in having dendrites that extend far away from their cell bodies. Mitochondria located in the dendrites can be separated from the nucleus for long distances. The mechanism of bigenomic coordination is of particular importance to cytochrome oxidase (CO), which has subunits that are encoded in both the nuclear and mitochondrial DNA. GA-binding protein (GABP) is a transcription factor that is required for the promoter activity of mitochondrial transcription factor A as well as several nuclear-encoded CO subunits. Thus, GABP may play a key role in coordinating the transcription of both mitochondrial and nuclear-encoded subunits of CO. The goal of the present study was to determine if GABP was expressed in neurons and whether and how it responded to increased neuronal activity. Using primary neuronal cultures, the beta-subunit of GABP was localized immunocytochemically to both the cytoplasm and the nucleus, whereas the alpha-subunit was expressed mainly in the nucleus. In KCl-treated cultures, immunoreactivity for both alpha- and beta-subunits was significantly increased in the nucleus compared with untreated sister cultures. The induction of GABP preceded that of CO gene expression from the two genomes, which, in turn, preceded that of CO activity. Thus, our data suggest that neuronal activity regulates subunit concentrations of GABP in the nucleus, and GABP may be a critical sensor of changes in neuronal activity. Our data are also consistent with the postulated role of GABP as a coordinator of both mitochondrial and nuclear transcription for subunits of CO in neurons. - Source: PubMed
Zhang CWong-Riley M T - Utrophin/dystrophin-related protein is the autosomal homologue of the chromosome X-encoded dystrophin protein. In adult skeletal muscle, utrophin is highly enriched at the neuromuscular junction. However, the molecular mechanisms underlying regulation of utrophin gene expression are yet to be defined. Here we demonstrate that the growth factor heregulin increases de novo utrophin transcription in muscle cell cultures. Using mutant reporter constructs of the utrophin promoter, we define the N-box region of the promoter as critical for heregulin-mediated activation. Using this region of the utrophin promoter for DNA affinity purification, immunoblots, in vitro kinase assays, electrophoretic mobility shift assays, and in vitro expression in cultured muscle cells, we demonstrate that ets-related GA-binding protein alpha/beta transcription factors are activators of the utrophin promoter. Taken together, these results suggest that the GA-binding protein alpha/beta complex of transcription factors binds and activates the utrophin promoter in response to heregulin-activated extracellular signal-regulated kinase in muscle cell cultures. These findings suggest methods for achieving utrophin up-regulation in Duchenne's muscular dystrophy as well as mechanisms by which neurite-derived growth factors such as heregulin may influence the regulation of utrophin gene expression and subsequent enrichment at the neuromuscular junction of skeletal muscle. - Source: PubMed
Khurana T SRosmarin A GShang JKrag T ODas SGammeltoft S