CREB2 TAD in vivo Kinase Assay Kit
- Known as:
- CREB2 TAD vivo Kinase Assay Kit
- Catalog number:
- LK0006
- Product Quantity:
- 10ug
- Category:
- Peptides
- Supplier:
- Panomics
- Gene target:
- CREB2 TAD vivo Kinase Assay Kit
Related genes to: CREB2 TAD in vivo Kinase Assay 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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- The silver pomfret (Pampus argenteus) represents a commercially vital marine fish species. However, its aquaculture potential, especially in temperate northern regions, is critically constrained by pronounced cold sensitivity. Building upon preliminary investigations which demonstrated a significant inverse correlation between dusp5 expression levels and ambient water temperature, this study aimed to elucidate the functional mechanism of dusp5-a cold-inducible dual-specificity phosphatase affecting the MAPK pathway-in mediating cold stress adaptation. Utilizing cellular models subjected to dusp5 knockdown (KO) and overexpression (OE), we systematically evaluated its impact on cold stress responses. Functional analysis revealed that dusp5 OE conferred significant cytoprotection: it effectively suppressed cold-induced DNA fragmentation indicative of apoptosis (quantified by TUNEL assay), ameliorated mitochondrial dysfunction (assessed via JC-1 staining and TEM ultrastructural examination), and diminished oxidative stress (indicated by reduced malondialdehyde/MDA levels). Subsequent qPCR profiling demonstrated that dusp5 OE modulated the expression of selected genes associated with MAPK signaling cascades, apoptotic pathways, endoplasmic reticulum (ER) stress response, and mitochondrial functional integrity under cold duress. Furthermore, employing dual-luciferase reporter assays, we identified atf2, atf4, jund, and stat1 as putative regulators of dusp5 promoter activity. Complementary histidine affinity chromatography facilitated the identification of candidate dusp5-associated proteins predominantly localized to the ER and mitochondrial compartments, with functional annotations implicating roles in ER homeostasis, autophagic processes, and peroxisome metabolism. Collectively, this work provides the preliminary mechanistic insights of dusp5 in promoting cold tolerance within P. argenteus, yielding novel and fundamental insights into the molecular regulators underpinning low-temperature adaptation mechanisms in marine teleosts. - Source: PubMed
Publication date: 2026/08/03
Tang MengkeZhang ManQiu YubeiLi YuanboDai QinqinChen XianglongWang ChongyangXu FangjunZhang LuYuan ZiYan XiaojunHu JiabaoWang Yajun - Type-I interferons (IFN-I) and IFN-stimulated genes (ISGs) are central to antiviral defense, while dysregulation can drive autoimmunity. expression is controlled by a highly ordered multiprotein complex composed of IRF3/7, NFκB, and ATF2/c-Jun (AP-1) that recruit coactivators and chromatin-remodeling proteins to expose the promoter for the RNA polymerase II (RNA Pol II) transcriptional machinery. Here, we identified the paraspeckle protein non-POU domain-containing octamer-binding protein (NONO) as a critical facilitator of innate immune activation. Loss of NONO enhanced replication of multiple orthoflaviviruses including West Nile virus due to impaired induction of IFN-I and ISGs. NONO did not affect upstream signaling but instead promoted chromatin accessibility and promoter access for RNA Pol II to drive expression of , ISGs, and proinflammatory cytokines. These findings position NONO as a key regulator of antiviral gene expression and reveal chromatin-levels of control that determine effective antiviral immunity. - Source: PubMed
Publication date: 2026/07/14
Hage AdamJanes MikhailaShue ByronMarkowitz Tovah EYoon SuhyeonShannon Jeffrey GBeare Paul ABroeckel Rebecca MLack Justin BMartens CraigBest Sonja M - 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