ZFP67 Western Blot Kit
- Known as:
- ZFP67 Western Blot Kit
- Catalog number:
- ARPK32749_T100
- Product Quantity:
- 25 Western Blots
- Category:
- -
- Supplier:
- ACR
- Gene target:
- ZFP67 Western Blot Kit
Related genes to: ZFP67 Western Blot Kit
- Gene:
- ZBTB7B NIH gene
- Name:
- zinc finger and BTB domain containing 7B
- Previous symbol:
- ZFP67
- Synonyms:
- ZBTB15, c-Krox, hcKrox, ZNF857B
- Chromosome:
- 1q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 2002-05-23
- Date modifiied:
- 2016-10-05
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- Hepatocarcinogenesis is a multi-step process. However, the regulators of hepatocellular carcinoma (HCC) initiation are understudied. Adult liver-specific gene expression was globally downregulated in HCC. We hypothesize that adult liver-specific genes, especially adult liver-enriched transcription factors may exert tumor-suppressive functions in HCC. In this study, we identify ZBTB7B, an adult liver-enriched transcription factor as a permissive regulator of HCC initiation. ZBTB7B is highly expressed in hepatocytes in adult livers, compared to fetal livers. To evaluate the functions of ZBTB7B in hepatocarcinogenesis, we performed hepatocyte-specific ZBTB7B knockout in hydrodynamic oncogene transfer-induced mouse liver cancer models. Hepatocyte-specific knockout of ZBTB7B promotes activated Akt and N-Ras-induced HCC development. Moreover, ZBTB7B deficiency sensitizes hepatocytes to a single oncogene Akt-induced oncogenic transformation and HCC initiation, which is otherwise incompetent in inducing HCC. ZBTB7B deficiency accelerates HCC initiation by down-regulating adult liver-specific gene expression and priming livers to a fetal-like state. The molecular mechanism underlying ZBTB7B functions in hepatocytes was investigated by integrated transcriptomic, phosphoproteomic, and chromatin immunoprecipitation-sequencing analyses. Integrative multi-omics analyses identify c-Jun as the core signaling node in ZBTB7B-deficient liver cancer initiation. c-Jun is a direct target of ZBTB7B essential to accelerated liver cancer initiation in ZBTB7B-deficient livers. Knockdown of c-Jun expression or dominant negative c-Jun expression delays HCC development in ZBTB7B-deficient livers. In addition, ZBTB7B competes with c-Jun for chromatin binding. Ectopic ZBTB7B expression attenuates the tumor-promoting functions of c-Jun. Expression of ZBTB7B signature, composed of 140 genes co-regulated by ZBTB7B and c-Jun, is significantly downregulated in early-stage HCCs compared to adjacent normal tissues, correlates to liver-specific gene expression, and is associated with good prognosis in human HCC. Thus, ZBTB7B functions as a permissive regulator of HCC initiation by directly regulating c-Jun expression and function. - Source: PubMed
Publication date: 2024/01/15
Zhu YueWang QinqinXie XinyuMa CuihongQiao YuemeiZhang YuWu YanjunGao YuanJiang JingLiu XinChen JianfengLi ChenGe Gaoxiang - Plant-derived exosome-like nanoparticles (PDENs) have been paid great attention in the treatment of ulcerative colitis (UC). As a proof of concept, we isolated and identified Portulaca oleracea L-derived exosome-like nanoparticles (PELNs) from edible Portulaca oleracea L, which exhibited desirable nano-size (~ 160 nm) and a negative zeta potential value (-31.4 mV). Oral administration of PELNs effectively suppressed the expressions of pro-inflammatory cytokines (TNF-α, IL-6, IL-12, and IL-1β) and myeloperoxidase (MPO), increased levels of the anti-inflammatory cytokine (IL-10), and alleviated acute colitis in dextran sulfate sodium (DSS)-induced C57 mice and IL-10 mice. Notably, PELNs exhibited excellent stability and safety within the gastrointestinal tract and displayed specific targeting to inflamed sites in the colons of mice. Mechanistically, oral administration of PELNs played a crucial role in maintaining the diversity and balance of gut microbiota. Furthermore, PELNs treatment enhanced Lactobacillus reuteri growth and elevated indole derivative levels, which might activate the aryl-hydrocarbon receptor (AhR) in conventional CD4 T cells. This activation downregulated Zbtb7b expression, leading to the reprogramming of conventional CD4 T cells into double-positive CD4CD8T cells (DP CD4CD8 T cells). In conclusion, our findings highlighted the potential of orally administered PELNs as a novel, natural, and colon-targeted agent, offering a promising therapeutic approach for managing UC. Schematic illustration of therapeutic effects of oral Portulaca oleracea L -derived natural exosome-like nanoparticles (PELNs) on UC. PELNs treatment enhanced Lactobacillus reuteri growth and elevated indole derivative levels, which activate the aryl-hydrocarbon receptor (AhR) in conventional CD4 T cells leading to downregulate the expression of Zbtb7b, reprogram of conventional CD4 T cells into double-positive CD4CD8T cells (DP CD4CD8 T cells), and decrease the levels of pro-inflammatory cytokines. - Source: PubMed
Publication date: 2023/08/31
Zhu Min-ZhengXu Hao-MingLiang Yu-JieXu JingYue Ning-NingZhang YuanTian Cheng-MeiYao JunWang Li-ShengNie Yu-QiangLi De-Feng - The transcription factor ThPOK (encoded by Zbtb7b) is well known for its role as a master regulator of CD4 lineage commitment in the thymus. Here, we report an unexpected and critical role of ThPOK as a multifaceted regulator of myeloid lineage commitment, differentiation and maturation. Using reporter and knockout mouse models combined with single-cell RNA-sequencing, progenitor transfer and colony assays, we show that ThPOK controls monocyte-dendritic cell versus granulocyte lineage production during homeostatic differentiation, and serves as a brake for neutrophil maturation in granulocyte lineage-specified cells through transcriptional regulation of lineage-specific transcription factors and RNA via altered messenger RNA splicing to reprogram intron retention. - Source: PubMed
Publication date: 2023/07/20
Basu JayatiOlsson AndreFerchen KyleTiterina Elizaveta KChetal KashishNicolas EmmanuelleCzyzewicz PhilipLevchenko DmitryGe LuHua XiangGrimes H LeightonSalomonis NathanKappes Dietmar J - One bottleneck in understanding the principles of 3D chromatin structures is caused by the paucity of known regulators. Cohesin is essential for 3D chromatin organization, and its interacting partners are candidate regulators. Here, we performed proteomic profiling of the cohesin in chromatin and identified transcription factors, RNA-binding proteins and chromatin regulators associated with cohesin. Acute protein degradation followed by time-series genomic binding quantitation and BAT Hi-C analysis were conducted, and the results showed that the transcription factor ZBTB21 contributes to cohesin chromatin binding, 3D chromatin interactions and transcriptional repression. Strikingly, multiomic analyses revealed that the other four ZBTB factors interacted with cohesin, and double degradation of ZBTB21 and ZBTB7B led to a further decrease in cohesin chromatin occupancy. We propose that multiple ZBTB transcription factors orchestrate the chromatin binding of cohesin to regulate chromatin interactions, and we provide a catalog of many additional proteins associated with cohesin that warrant further investigation. - Source: PubMed
Wang RuiXu QiqinWang ChenluTian KaiWang HuiJi Xiong - Naive CD4 T cells are more resistant to age-related loss than naive CD8 T cells, suggesting mechanisms that preferentially protect naive CD4 T cells during aging. Here, we show that TRIB2 is more abundant in naive CD4 than CD8 T cells and counteracts quiescence exit by suppressing AKT activation. TRIB2 deficiency increases AKT activity and accelerates proliferation and differentiation in response to interleukin-7 (IL-7) in humans and during lymphopenia in mice. TRIB2 transcription is controlled by the lineage-determining transcription factors ThPOK and RUNX3. Ablation of Zbtb7b (encoding ThPOK) and Cbfb (obligatory RUNT cofactor) attenuates the difference in lymphopenia-induced proliferation between naive CD4 and CD8 cells. In older adults, ThPOK and TRIB2 expression wanes in naive CD4 T cells, causing loss of naivety. These findings assign TRIB2 a key role in regulating T cell homeostasis and provide a model to explain the lesser resilience of CD8 T cells to undergo changes with age. - Source: PubMed
Publication date: 2023/03/06
Cao WenqiangSturmlechner InesZhang HuiminJin JunHu BinJadhav Rohit RFang FengqinWeyand Cornelia MGoronzy Jörg J