CREB1_BOVIN CREB2 ELISA tesk kit
- Known as:
- CREB1_BOVIN CREB2 Enzyme-linked immunosorbent assay test tesk reagent
- Catalog number:
- gen16956
- Product Quantity:
- 1
- Category:
- Peptides
- Supplier:
- Other suppliers
- Gene target:
- CREB1_BOVIN CREB2 ELISA tesk kit
Related genes to: CREB1_BOVIN CREB2 ELISA tesk kit
- Gene:
- ATF2 NIH gene
- Name:
- activating transcription factor 2
- Previous symbol:
- CREB2
- Synonyms:
- TREB7, CRE-BP1, HB16
- Chromosome:
- 2q31.1
- Locus Type:
- gene with protein product
- Date approved:
- 1991-08-01
- Date modifiied:
- 2016-10-05
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- Renal cell carcinoma (RCC) is a common and highly lethal malignancy. Tribbles pseudokinase 3 (TRIB3) has been reported to exert oncogenic roles in the pathogenesis of multiple tumors; nevertheless, the detailed mechanisms through which TRIB3 drives RCC development remain largely undefined. In this study, qPCR and Western blot were used to quantify the levels of TRIB3, STIP1 homology and U-box containing protein 1 (STUB1), and activating transcription factor 2 (ATF2). Cell proliferation, invasion, stemness, and angiogenic capacity were assessed by MTT assay, flow cytometry, Transwell invasion assay, sphere-formation assay, and tube-formation assay, respectively. The interaction between TRIB3 and STUB1 was examined by co-immunoprecipitation (Co-IP), and the relationship between TRIB3 and ATF2 was verified using dual-luciferase reporter assays. A xenograft model was employed to evaluate the tumorigenic potential of RCC cells upon STUB1 overexpression. The study found that TRIB3 expression was markedly elevated in RCC. Knockdown of TRIB3 profoundly inhibited cell proliferation, invasion, migration, and stem-like properties, while simultaneously inducing apoptosis and promoting ferroptosis. TRIB3 physically interacted with STUB1 and was poly-ubiquitinated and degraded by this E3 ligase; consequently, STUB1 overexpression suppressed RCC progression both in vitro and in vivo by targeting TRIB3. Conversely, ATF2 transcriptionally activated TRIB3 expression, and enforced TRIB3 expression partially rescued the inhibitory effects of ATF2 knockdown in RCC cells. Collectively, these findings demonstrate that TRIB3 drives RCC progression; STUB1 curbs RCC by degrading TRIB3, whereas ATF2 promotes RCC via transcriptional activation of TRIB3. Thus, modulating TRIB3 expression may offer a novel therapeutic strategy for RCC. - Source: PubMed
Publication date: 2026/07/15
Wang WeiZhang LongWu TaoLi YuefengWang HaidongHuang HaiqiaoGuo Yuexian - Gemcitabine (GEM) is a cornerstone of chemotherapy for lung adenocarcinoma (LUAD). However, acquired resistance severely limits its clinical efficacy, leading to relapse and metastasis. This study aims to investigate the role of KNSTRN in GEM resistance and its underlying molecular mechanisms in LUAD. Bioinformatics analysis revealed the expression levels of KNSTRN in LUAD tissues and the enriched pathways, and analyzed the prognostic impact of KNSTRN in LUAD, predicting the upstream transcription factor (TF) ATF2. The study examined the correlation and binding sites between KNSTRN and ATF2, as well as the expression of ATF2 in LUAD tissues. Molecular and cellular experiments were conducted to depict the binding relationship between ATF2 and KNSTRN and their expression within cells; to assess cell viability and IC values; to evaluate the expression of proteins related to the mismatch repair pathway, glycolytic pathway, and DNA damage markers; and to measure extracellular acidification rate, oxygen consumption rate, lactate production, and glucose consumption. Bioinformatics evidence pointed to ATF2 being the upstream TF for KNSTRN, with their expressions positively linked. High levels of ATF2 and KNSTRN were detected in LUAD tissues and cells, and high KNSTRN expression was associated with poor prognosis. KNSTRN promoted glycolysis and lactate accumulation, which in turn suppressed the expression of key MMR components MLH1 and MSH2, thereby impairing DNA damage repair capacity correlated positively with the expression of pivotal genes in these pathways. Molecular and cellular studies corroborated that KNSTRN overexpression enhances GEM resistance, a process that is thought to be mediated by increased lactate production and the regulation of mismatch repair pathways. Rescue experiments showed that the overexpression of KNSTRN reversed the effects of ATF2 silencing on LUAD cell GEM resistance. This study has uncovered a novel mechanism by which ATF2 activates KNSTRN, leading to increased lactate production and the downregulation of MLH1 and MSH2 expression, key components of the mismatch repair machinery, thereby promoting GEM resistance in LUAD. This discovery offers new insights for improving the efficacy of chemotherapy in LUAD. - Source: PubMed
Wu HuanghuiHan KunZheng BiaolongXiao Tingting - LncRNAs emerge as critical regulators of gene expression and epigenetic modulation in human cancer. However, the biological and clinical significance of the lncRNA in differentiated thyroid cancers (DTCs) remains poorly understood. - Source: PubMed
Publication date: 2026/06/08
Murugan Avaniyapuram KannanAl-Hindi HindiAlzahrani Ali S - Long COVID affects hundreds of millions of individuals worldwide, yet its underlying biological mechanisms remain incompletely understood, and the absence of validated biomarkers continues to limit diagnosis and clinical management. Most biomarker studies have focused on hospitalized patients with severe disease, leaving non-hospitalized populations, particularly healthcare workers, who are at high occupational risk, underrepresented. This gap may constrain the identification of biomarkers relevant to milder but persistent post-acute phenotypes. - Source: PubMed
Publication date: 2026/06/04
Espín EstefaníaYang ChengliangShannon Casey PCheckervarty Abhinav KKim SehyeonLapp LindaAssadian SaraGrunau BrianGoldfarb David MHutton JacobHuan TaoTebbutt Scott J - To explore the predictive value of miR-451-5p in delayed fracture healing (DFH) and its mechanism of action in fracture healing. Patients with normal fracture healing (NFH) and DFH were included in this study. The expression of miR-451-5p in serum was detected by RT-qPCR. The predictive potential of miR-451-5p for DFH was evaluated by ROC analysis, and risk factors influencing DFH were determined using logistic regression analysis. The proliferation, apoptosis and expression levels of osteogenic differentiation markers (ALP, BMP2, OSX) of mouse embryonic osteoblast precursor cells (MC3T3-E1) were detected by CCK-8, flow cytometry, RT-qPCR and western blot. The targeting relationship between miR-451-5p and ATF2 was verified by dual-luciferase reporter assay and RNA pull-down experiments. The level of miR-451-5p in the serum of DFH patients was significantly higher than that in the NFH group. Its sensitivity for predicting DFH was 81.33%, and its specificity was 86.96%. miR-451-5p is an independent risk factor for DFH. Overexpression of miR-451-5p could inhibit the proliferation of osteogenic precursor cells, promote cell apoptosis, and downregulate the expression of osteogenic differentiation markers. miR-451-5p binds to ATF2 and inhibits its expression. Overexpression of ATF2 could reverse the inhibitory effect of miR-451-5p on osteogenic differentiation. During the process of osteogenesis, miR-451-5p negatively regulates cell proliferation and osteogenesis by inhibiting the function of ATF2. Clinically, miR-451-5p has the potential to serve as a biomarker for the early predictive of DFH. - Source: PubMed
Publication date: 2026/06/19
Qu ChuangyeBao WeibingWang WenqiZhu Xiaozhong