ZNF297B antibody - N-terminal region (ARP31799_T100)
- Known as:
- ZNF297B (anti-) - N-terminal region (ARP31799_T100)
- Catalog number:
- arp31799_t100
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- ZNF297B antibody - N-terminal region (ARP31799_T100)
Related genes to: ZNF297B antibody - N-terminal region (ARP31799_T100)
- Gene:
- ZBTB43 NIH gene
- Name:
- zinc finger and BTB domain containing 43
- Previous symbol:
- ZNF297B
- Synonyms:
- KIAA0414, ZNF-X, FLJ22470, ZBTB22B
- Chromosome:
- 9q33.3
- Locus Type:
- gene with protein product
- Date approved:
- 2002-01-29
- Date modifiied:
- 2015-08-26
Related products to: ZNF297B antibody - N-terminal region (ARP31799_T100)
Related articles to: ZNF297B antibody - N-terminal region (ARP31799_T100)
- Purine-pyrimidine repeats (PPRs) can form left-handed Z-form DNA and induce DNA double-strand breaks (DSBs), posing a risk for genomic rearrangements and cancer. The zinc finger (ZF) and BTB domain-containing protein 43 (ZBTB43) is a transcription factor containing two Cys2-His2 (C2H2) and one C3H1 zinc fingers and plays a crucial role in maintaining genomic and epigenomic integrity by converting mutagenic Z-form PPRs to the B-form in prospermatogonia. Despite its importance, the molecular mechanism underlying the recognition of PPRs by ZBTB43 remains elusive. In this study, we determined the X-ray crystal structure of the ZBTB43 ZF1-3 in complex with the B-form DNA containing the CA repeats sequence. The structure reveals that ZF1 and ZF2 primarily recognize the CACA sequence through specific hydrogen-bonding and van der Waals contacts via a quadruple center involving Arg389, Met411, His413, and His414. These interactions were further validated by fluorescence-based DNA-binding assays using mutated ZBTB43 variants. Our structural investigation provides valuable insights into the recognition mechanism of PPRs by ZBTB43 and suggests a potential role for ZBTB43 in the transformation of Z-DNA to B-DNA, contributing to the maintenance of genomic stability. - Source: PubMed
Publication date: 2024/09/29
Yang YangZhang ShutingXu LiPan YanXuan YumiKai YuanzhongChen Xuemin - Background Neurotrophic tropomyosin receptor kinase (NTRK) gene fusions are found in 1% of gliomas across children and adults. TRK inhibitors are promising therapeutic agents for NTRK-fused gliomas because they are tissue agnostic and cross the blood-brain barrier (BBB). Methods We investigated twelve NGS-verified NTRK-fused gliomas from a single institute, Seoul National University Hospital. Results The patient cohort included six children (aged 1-15 years) and six adults (aged 27-72 years). NTRK2 fusions were found in ten cerebral diffuse low-grade and high-grade gliomas (DLGGs and DHGGs, respectively), and NTRK1 fusions were found in one cerebral desmoplastic infantile ganglioglioma and one spinal DHGG. In this series, the fusion partners of NTRK2 were HOOK3, KIF5A, GKAP1, LHFPL3, SLMAP, ZBTB43, SPECC1L, FKBP15, KANK1, and BCR, while the NTRK1 fusion partners were TPR and TPM3. DLGGs tended to harbour only an NTRK fusion, while DHGGs exhibited further genetic alterations, such as TERT promoter/TP53/PTEN mutation, CDKN2A/2B homozygous deletion, PDGFRA/KIT/MDM4/AKT3 amplification, or multiple chromosomal copy number aberrations. Four patients received adjuvant TRK inhibitor therapy (larotrectinib, repotrectinib, or entrectinib), among which three also received chemotherapy (n = 2) or proton therapy (n = 1). The treatment outcomes for patients receiving TRK inhibitors varied: one child who received larotrectinib for residual DLGG maintained stable disease. In contrast, another child with DHGG in the spinal cord experienced multiple instances of tumour recurrence. Despite treatment with larotrectinib, ultimately, the child died as a result of tumour progression. An adult patient with glioblastoma (GBM) treated with entrectinib also experienced tumour progression and eventually died. However, there was a successful outcome for a paediatric patient with DHGG who, after a second gross total tumour removal followed by repotrectinib treatment, showed no evidence of disease. This patient had previously experienced relapse after the initial surgery and underwent autologous peripheral blood stem cell therapy with carboplatin/thiotepa and proton therapy. Conclusions Our study clarifies the distinct differences in the pathology and TRK inhibitor response between LGG and HGG with NTRK fusions. - Source: PubMed
Publication date: 2024/07/16
Kim Eric EunshikPark Chul-KeeKim Seung-KiPhi Ji HoonPaek Sun HaChoi Jung YoonKang Hyoung JinLee Joo HoWon Jae KyungYun HongseokPark Sung-Hye - The impact of cardiovascular disease (CVD) risk factors, encompassing various biological determinants and unhealthy lifestyles, on the functional dynamics of circulating monocytes-a pivotal cell type in CVD pathophysiology remains elusive. In this study, we aimed to elucidate the influence of CVD risk factors on monocyte transcriptional responses to an infectious stimulus. - Source: PubMed
Publication date: 2024/02/12
Lu ChangDonners Marjo M P Cde Baaij Julius B JJin HanOtten Jeroen J TManca Marcovan Zonneveld Anton JanJukema J WouterKraaijeveld AdriaanKuiper JohanPasterkamp GerardMees BarendSluimer Judith CCavill RachelKarel Joël M HGoossens PieterBiessen Erik A L - Exercise and caloric restriction (CR) significantly increase longevity across a range of species and delay aging-related losses in organ function. Although both interventions enhance skeletal muscle function, the molecular mechanisms underlying these associations are unknown. We sought to identify genes regulated by CR and exercise in muscle, and investigate their relationship with muscle function. To do this, expression profiles of Gene Expression Omnibus datasets obtained from the muscle tissue of calorie-restricted male primates and young men post-exercise were analyzed. There were seven transcripts (, , , , , and ) that were consistently upregulated by both CR and exercise training. We used C2C12 murine myoblasts to investigate the effect of silencing these genes on myogenesis, mitochondrial respiration, autophagy, and insulin signaling, all of which are processes affected by CR and exercise. Our results show that in C2C12 cells, and expression were critical for myogenesis, and five genes (, , , , and ) regulated mitochondrial respiration while having no effect on autophagy. knockdown increased the expression of genes involved in muscle atrophy and induced myotube atrophy. These findings suggest new resources for studying the mechanisms underlying the beneficial effects of exercise and calorie restriction on skeletal muscle function and lifespan extension. - Source: PubMed
Publication date: 2023/06/12
Kang Jae SookKim Min JuKwon Eun-SooLee Kwang-PyoKim ChunaKwon Ki-SunYang Yong Ryoul - We recently discovered a novel biological process, the scheduled remodeling of Z-DNA structures in the developing fetal mouse male germ cells [Nat. Cell Biol. 24, 1141-1153]. This process affects purine/pyrimidine dinucleotide repeat (PPR) rich sequences, which can form stable left-handed Z-DNA structures. The protein that carries out this function is identified as ZBTB43, member of a large family of ZBTB proteins. Z-DNA remodeling by ZBTB43 not only coincides with global remodeling of DNA methylation and chromatin events in the male germ line, but it also is a prerequisite for de novo DNA methylation. When ZBTB43 changes DNA structure from the left-handed zigzag shaped Z-DNA to the regular smooth right-handed B-DNA, it also generates a suitable substrate for the de novo DNA methyltransferase, DNMT3A. By instructing de novo DNA methylation at PPRs in prospermatogonia, ZBTB43 safeguards epigenomic integrity of the male gamete. PPRs are fragile sequences, sites of large deletions and rearrangements in mammalian cells, and this fragility is thought to be due to Z-DNA structure formation rather than the sequence itself. This idea is now supported by the in vivo finding that DNA double strand breaks accumulate in mutant prospermatogonia which lack ZBTB43-dependent Z-DNA remodeling. If unrepaired, double stranded DNA breaks can lead to germ line mutations. Therefore, by preventing such breaks ZBTB43 is critical for guarding genome stability between generations. Here, we discuss the significance and implications of these findings in more detail. - Source: PubMed
Meng YingyingSzabó Piroska E