CREBZF Antibody
- Known as:
- CREBZF Antibody
- Catalog number:
- GWB-MM252I
- Product Quantity:
- 50ug
- Category:
- -
- Supplier:
- GenWay
- Gene target:
- CREBZF Antibody
Related genes to: CREBZF Antibody
- Gene:
- CREBZF NIH gene
- Name:
- CREB/ATF bZIP transcription factor
- Previous symbol:
- -
- Synonyms:
- ZF
- Chromosome:
- 11q14.1
- Locus Type:
- gene with protein product
- Date approved:
- 2006-11-13
- Date modifiied:
- 2014-11-19
Related products to: CREBZF Antibody
Related articles to: CREBZF Antibody
- Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by persistent inflammation and progressive joint damage. This study investigated the role of microRNA-223 (miR-223) in RA and evaluated the therapeutic effects of triptolide (Tri), a diterpenoid epoxide derived from the traditional Chinese medicinal herb . A collagen-induced arthritis (CIA) mouse model was used to assess the effects of Tri and methotrexate (MTX). Micro-computed tomography, histological staining, enzyme-linked immunosorbent assay, flow cytometry, RT-qPCR, and western blot analysis were used to evaluate joint damage, inflammation, cytokine profiles, miR-223 expression, and the function of CREBZF, a downstream target of miR-223. CIA mice exhibited marked joint inflammation, swelling, bone erosion, and inflammatory cell infiltration, increased pro-inflammatory cytokine levels, and elevated miR-223 expression. Tri and MTX ameliorated these abnormalities and protected against bone erosion and inflammation. Tri suppressed the disease-associated elevation of miR-223, attenuated pathological fibroblast-like synoviocyte (RA-FLS) phenotypes, and shifted cytokine profiles toward an anti-inflammatory state. Dual-luciferase reporter and AGO2-RIP-qPCR assays supported direct regulation of CREBZF by miR-223. Tri restored CREBZF expression and inhibited NF-κ B signaling, thereby reducing RA-FLS proliferation and promoting apoptosis. These findings indicate that Tri ameliorates RA, at least partly, through the miR-223/CREBZF axis and identify this pathway as a potential therapeutic target. - Source: PubMed
Publication date: 2026/08/21
Liu Xiao-BaoXiang Ying-XingYang Jia-HaoZou Fang-ShuShi Mei-FengChen Xue-QingLin Chang-SongXu QiangLiu Min-Ying - Regulatory T (Treg) cells in visceral adipose tissue (VAT) play essential roles in systemic metabolic homeostasis under distinct physiological and pathological conditions. However, the metabolic cues that drive Treg cell subset specialization in the obese VAT niche remain elusive. Here, we demonstrated that palmitic acid instigated chronic VAT inflammation and systemic metabolic disturbance by compromising the immunosuppressive function of the ICOShi Treg subset. Palmitic acid, but not oleic acid, activated Crebzf expression in VAT Treg cells from HFHS diet-induced obese and ob/ob mice. Crebzf deficiency significantly attenuated diet-induced obesity and inflammation by upregulating the suppressive function of VAT ICOShi Treg cells. Moreover, adoptive transfer of Crebzf-deficient ICOShi Treg cells into Rag1-/- mice alleviated HFHS diet-induced inflammation and metabolic disorders more effectively than transfer of Crebzf-sufficient ICOShi Treg cells. Mechanistically, CREBZF interacted with c-JUN to inhibit Foxp3 activity, thereby impairing the stability and inhibitory cytokine production of ICOShi Treg cells. In human subjects, CREBZF levels in VAT Treg cells were elevated and negatively correlated with FOXP3 activity. Collectively, these findings uncover a specific ICOShi Treg subset that responds to palmitic acid, thereby coupling obesogenic signals to VAT remodeling and systemic metabolic homeostasis. - Source: PubMed
Publication date: 2026/07/23
Su WeitongLiu YuxiaoYan XiHuang MengyaoXu LinghaoLin JingChen XufengHu PuyuanGao ChenlinWen JianWang HongdongDing DongZheng ZengpengLi WenjingLi LianjiaLiu ZhanQian KeyuGao JingZhang TingtingMao XiaobingZhang HaibingLu WeiLi BinLi HongCui AoyuanBi YanZhang ChunxiangLi Yu - Ovarian secretion of steroid hormones is crucial for female reproductive health. CREBZF, a basic leucine zipper transcription factor, can heterodimerize with other transcription factors to regulate genes involved in various biological processes. This study investigates the role of CREBZF in female reproduction and steroid hormone synthesis regulation. Whole ovarian knockout of CREBZF affects the estrous cycle, antral follicle development, and testosterone and estradiol levels in female mice. Conditional knockout of CREBZF in Cyp17a1-positive cells results in altered serum testosterone during estrus, impaired postpartum maternal behavior, and significantly reduced offspring survival, associated with abnormal corticosterone and oxytocin levels. In NCI-H295R cells induced for steroidogenesis, CREBZF knockdown reduced testosterone and corticosterone secretion. RNA sequencing of CREBZF-knockdown NCI-H295R cells identified 51 differentially expressed genes enriched in steroidogenesis-related pathways. CREBZF knockdown also reduced c-Jun and ApoE expression, with a significant decrease in intracellular cholesterol. CREBZF interacts with c-Jun and binds to the ApoE promoter to regulate expression. Database screening identified two CREBZF/c-Jun binding sites, where CREBZF enhances c-Jun-mediated activation of ApoE at Site1 ( 299 to 286 bp), but inhibits it at Site2 (+70 to +83 bp). In conclusion, the CREBZF/c-Jun complex regulates ApoE expression, influencing cholesterol levels and female steroidogenesis, which is crucial for reproductive function. - Source: PubMed
Niu Hong-YuLi ChaoZhang Rui-HangDu Mu-ZiWuen Ji-YaLiu Hao-KunLi Zu-HuiWang Ai-HuaJin Ya-PingLin Peng-Fei - Osteoarthritis (OA) is a degenerative joint disease caused by the breakdown of joint cartilage and adjacent bone. Joint injury, being overweight, differences in leg length, high levels of joint stress, abnormal joint or limb development, and inherited factors have been implicated in the etiology of OA. In addition to physical damage to the joint, a role for inflammatory processes has been identified as well. Small heterodimer partner-interacting leucine zipper protein (SMILE) regulates transcription and many cellular functions. Among the proteins activated by SMILE is the peroxisome proliferator-activated receptor (PPAR) γ, which mediates the activities of CD4 + T helper cells, including Th1, Th2, and Th17, as well as Treg cells. PPAR-γ binds to STAT3 to inhibit its transcription, thereby suppressing the expression of the NF-κB pathway, and in turn, the expression of the inflammatory cytokines interferon (IFN), interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α, which are sub-signals of STAT3 and NF-κB. - Source: PubMed
Publication date: 2024/11/12
Moon JeonghyeonCho Keun-HyungJhun JooYeonChoi JeongWonNa Hyun-SikLee Jeong SuLee Seung YoonMin Jun-KiShetty AnanPark Sung-HwanKim Seok JungCho Mi-La - Quantum dots have diverse biomedical applications, from constructing biological infrastructures like medical imaging to advancing pharmaceutical research. However, concerns about human health arise due to the toxic potential of quantum dots based on heavy metals. Therefore, research on quantum dots has predominantly focused on oxidative stress, cell death, and other broader bodily toxicities. This study investigated the toxicity and cellular responses of mouse embryonic stem cells (mESCs) and mouse adult stem cells (mASCs) to nitrogen-doped carbon quantum dots (NCQDs) made of non-metallic materials. Cells were exposed to NCQDs, and we utilized a fluorescent ubiquitination-based cell system to verify whether NCQDs induce cytotoxicity. Furthermore, we validated the differentiation-inducing impact of NCQDs by utilizing embryonic stem cells equipped with the Oct4 enhancer-GFP reporter system. By analyzing gene expression including Crebzf, Chop, and ATF6, we also observed that NCQDs robustly elicited endoplasmic reticulum (ER) stress. We confirmed that NCQDs induced cytotoxicity and abnormal differentiation. Interestingly, we also confirmed that low concentrations of NCQDs stimulated cell proliferation in both mESCs and mASCs. In conclusion, NCQDs modulate cell death, proliferation, and differentiation in a concentration-dependent manner. Indiscriminate biological applications of NCQDs have the potential to cause cancer development by affecting normal cell division or to fail to induce normal differentiation by affecting embryonic development during pregnancy. Therefore, we propose that future biomedical applications of NCQDs necessitate comprehensive and diverse biological studies. - Source: PubMed
Publication date: 2024/10/02
Song Hyun HeeChoi HyunwooKim SeonghanKim Hwan GyuAn SangminKim SejungJang Hoon