BCL6 Antibody - C-terminal region (ARP31838_P050)
- Known as:
- BCL6 Antibody - C-terminal region (ARP31838_P050)
- Catalog number:
- arp31838_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- BCL6 Antibody - C-terminal region (ARP31838_P050)
Related genes to: BCL6 Antibody - C-terminal region (ARP31838_P050)
- Gene:
- BCL6 NIH gene
- Name:
- BCL6 transcription repressor
- Previous symbol:
- ZNF51
- Synonyms:
- ZBTB27, LAZ3, BCL5, BCL6A
- Chromosome:
- 3q27.3
- Locus Type:
- gene with protein product
- Date approved:
- 1993-04-12
- Date modifiied:
- 2019-01-25
Related products to: BCL6 Antibody - C-terminal region (ARP31838_P050)
Related articles to: BCL6 Antibody - C-terminal region (ARP31838_P050)
- Diffuse large B-cell lymphoma (DLBCL) is the most common subtype of malignant lymphoma in adults. According to the gene expression profile, it can be classified into germinal center B-cell (GCB) type and activated B-cell (ABC) type. Cases with coexistence of the two subtypes and cross-site involvement are extremely rare. Herein, we report a 65-year-old female patient who presented with blurred vision in the right eye. Imaging examinations revealed space-occupying lesions in the left thalamus, basal ganglia, deep temporal lobe and left temporal muscle. Pathological biopsy and immunohistochemistry confirmed that the intracranial lesion was ABC subtype DLBCL and the temporal muscle lesion was GCB subtype DLBCL. Fluorescence hybridization (FISH) excluded c-MYC, Bcl-2 and Bcl-6 gene rearrangements. No involvement of other sites was detected by PET-CT and bone marrow biopsy. The patient initially received 2 cycles of rituximab combined with high-dose methotrexate chemotherapy. Efficacy evaluation showed stable disease (SD) of the intracranial lesion and complete response (CR) of the temporal muscle lesion. Subsequently, the regimen was adjusted to 6 cycles of cytarabine combined with temozolomide chemotherapy followed by radiotherapy for the intracranial lesion. Eventually, the intracranial lesion achieved partial response (PR) and the temporal muscle lesion maintained sustained CR. Up to the date of follow-up, the patient's condition was stable without recurrence. Combined with literature review, this article discusses the possible mechanisms of the coexistence of dual-subtype DLBCL (clonal evolution or biclonal origin), the potential pathways of temporal muscle metastasis and the impact of subtype differences on treatment response, which provides clinical reference for the diagnosis and individualized treatment of such rare cases. - Source: PubMed
Publication date: 2026/04/01
Liu YadongDuan XuejuanLiu JinlongChen ChenYin ShaoningCheng GangYang MeijianHan WeiLi NaZhang XianboZhao Jing - We previously showed that ZDHHC11 promotes cell growth in Burkitt lymphoma (BL). To explore the underlying mechanism, we performed a genome-wide gene expression analysis upon ZDHHC11 knockdown. We identified MEF2B, a transcription factor critical for germinal center formation, as a downstream target and validated repression of MEF2B at the RNA and protein level upon ZDHHC11 knockdown in BL cell lines. The relevance of MEF2B was shown upon its knockdown, which strongly inhibited growth of BL cells. Since MEF2B is a known regulator of BCL6 in normal GC B-cells, diffuse large B-cell lymphoma, and follicular lymphoma, we subsequently focused on the effect of MEF2B knockdown on BCL6. We observed a strong decrease in BCL6 at the RNA and protein level in BL and showed a strong correlation between MEF2B and BCL6 transcript levels in a panel of B-cell lymphoma cell lines, primary BL samples, and normal B-cell subsets. Knockdown of BCL6 also strongly inhibited growth of BL cell lines, whereas BCL6 overexpression partially rescued the growth-inhibitory effect of MEF2B knockdown. Together, our data indicate that ZDHHC11 promotes BL cell growth at least in part by stimulating expression of MEF2B, which promoted BL cell survival through both BCL6-dependent and independent pathways. Our work highlighted the importance of the MEF2B-BCL6 axis, which strongly supports BL growth and identified ZDHHC11 as a novel regulator of this axis. - Source: PubMed
Publication date: 2026/04/16
Ziel-Swier Lotteke J Y MRassek KarolinaLiu YichenSeitz AnnikaKoerts Jasperde Jong DeboraRutgers BeaKompaniiets AnastasiiaPrzybył JuliaChamuleau Martine E Dvan den Berg AnkeDzikiewicz-Krawczyk AgnieszkaKluiver Joost - The rate of orthodontic tooth movement (OTM) directly influences the duration of orthodontic treatment. OTM relies on the bone modeling under mechanical stress, wherein osteoclasts mediate bone resorption. Bcl6 and STAT1 serve as critical regulatory factors in the osteoclast differentiation pathway. This study aims to elucidate how Bcl6 and STAT1 interact to regulate osteoclast differentiation. - Source: PubMed
Publication date: 2026/04/16
Ma XinyuanChen ShuigeChen YuetongWang YugeLin ChenZhang Linkun - The transcriptional repressor B cell lymphoma 6 (BCL6) is highly expressed in skeletal muscle. Although transcriptome-wide studies have shown BCL6 dysregulation in muscular dystrophies, investigations into its endogenous roles in muscle biology remain scarce. We therefore generated skeletal muscle-specific Bcl6 knockout (M-Bcl6 KO) mice and used adeno-associated virus to knockdown (KD) Bcl6 selectively in limb muscles of mice. In both models, Bcl6 deficiency led to reduced muscle mass and contractility. Single-nucleus RNA sequencing and biochemical analyses revealed upregulation of Socs2, and inhibition of the IGF1/AKT pathway. Mitochondrial respiration was significantly reduced in permeabilized myofibers upon Bcl6 KO and KD, and electron microscopy showed decreased mitochondrial density and altered morphology. Pathways regulating mitochondrial quality control were also downregulated. While Bcl6 KO did not significantly impair baseline treadmill running capacity, it blunted the adaptive response to endurance training. These findings demonstrate that Bcl6 is a critical regulator of skeletal muscle mass and mitochondrial bioenergetics, acting through transcriptional control of signaling and metabolic pathways essential for the maintenance of muscle mass and function. - Source: PubMed
Publication date: 2026/04/13
Usmani Shirine ELeduc-Gaudet Jean-PhilippeChau StephanieBellissimo Catherine AVohra ShabanaDesjardins KrystelPollock-Tahiri EvanShi IrisaChun FeliceCapobianco AnthonyDelisle PascaleDupebe WandaCefis MarinaMarcangeli VincentGhebreselassie MarthaLiang Yu-ChengSeki YasufumiMayaki DominiqueHussain SabahGoligher EwanKapoor MohitLocke MariusGouspillou GillesWoo Minna - - Source: PubMed
Perkins BryantHale J Scott