MKK7 (Constitutively Active) Recombinant Adenovirus
- Known as:
- MKK7 (Constitutively Active) Recombinant Adenovirus
- Catalog number:
- ADV-128
- Product Quantity:
- 50
- Category:
- -
- Supplier:
- Cell Biolabs
- Gene target:
- MKK7 (Constitutively Active) Recombinant Adenovirus
Related genes to: MKK7 (Constitutively Active) Recombinant Adenovirus
- Gene:
- MAP2K7 NIH gene
- Name:
- mitogen-activated protein kinase kinase 7
- Previous symbol:
- PRKMK7
- Synonyms:
- MKK7, Jnkk2
- Chromosome:
- 19p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1998-04-28
- Date modifiied:
- 2016-10-05
Related products to: MKK7 (Constitutively Active) Recombinant Adenovirus
Related articles to: MKK7 (Constitutively Active) Recombinant Adenovirus
- To discover novel anti-cancer agents, a total of twenty derivatives of 8-hydroxyquinoline were synthesized by alkylation and benzylation of 8-hydroxyl-5,7-dibromo-2-methylquinoline. The anti-cancer activity of these compounds against triple-negative breast cancer (TNBC) cells MDA-MB-468, lung cancer cells A549, and liver cancer cells HepG2 were evaluated using MTT assay. Among them, compounds 10k and 10l exhibited profound effects against MDA-MB-468 cells with IC values less than 1 μM. The most potent one, compound 10l, was found to significantly inhibit the proliferation and migration of MDA-MB-468 cells. It also induced apoptosis in MDA-MB-468 cells, as evidenced by Hoechst staining, flow cytometry, and Western blot analysis. Treatment with 10l significantly increased phospho-JNK (p-JNK) levels, and blockage of JNK signaling by either pharmacological inhibitor SP600125 or JNK siRNA abolished its pro-apoptotic effect, demonstrating that JNK activation was critical for 10l-induced cell death. Notably, the major kinase upstream of JNK MKK7 was activated under 10l treatment. All these data suggested that compound 10l was capable of inducing apoptosis via activating MKK7-JNK pathway, supporting its potential as a therapeutic candidate for TNBC treatment. - Source: PubMed
Publication date: 2025/10/17
Ma LiangZhang ShizhunMao XiupingLu ZhigangTong ZixuanGuo JunhuiHu JunfengChang KailiLiu ZiHuang Guozheng - Triplophysa yarkandensis is an economically important fish species native to the Tarim River of Xinjiang, China. Amid ongoing climate warming and rising temperatures in the Tarim River, T. yarkandensis has demonstrated a degree of physiological adaptation to heat stress. However, the underlying mechanisms of this thermal adaptation and the impact of high-temperature stress on gene expression profiles remain poorly understood. Investigating its heat tolerance genes can aid in protecting wild populations from the threat of endangerment due to ecological damage. Based on the optimal growth temperature and maximum heat tolerance of T. yarkandensis, 20°C was used as the normal temperature control group (NT20), while 27 and 34°C served as the heat treatment groups (HT27 and HT34). In this study, 9544 differentially expressed genes (DEGs) were identified, comprising 4823 upregulated and 4861 downregulated genes in muscle tissue. Several heat-related genes, such as hspa5, hsp70, hyou1, hsp40, atp2a and cacna1a, were identified. These genes were primarily enriched in pathways such as spinocerebellar ataxia, protein processing in endoplasmic reticulum and the legionellosis signalling pathway. Quantitative real-time PCR analysis was employed to verify the significantly expressed DEGs, and the results aligned with the trends observed in transcriptome analysis. Key genes including ire1, traf2, map3k5, map2k7, jnk, bax, bcl2 and capn1 enriched in protein processing in endoplasmic reticulum were quantitatively analysed. In this study, we employed transcriptomic analysis combined with bioinformatics approaches to explore the molecular responses of T. yarkandensis under heat stress. The findings contribute to the conservation of its germplasm resources, support the breeding of heat-tolerant strains, and provide a scientific basis for artificial propagation and stock enhancement efforts. - Source: PubMed
Publication date: 2025/09/18
Wang XiyaoChen ShengaoLi YaoyaoZhang HaiguangCui DongLiu YimengLiu Yunguo - CDK4/6 inhibitors in combination with endocrine therapy are now used as front-line treatment for patients with estrogen-receptor positive (ER+) breast cancer. While this combination improves overall survival, the mechanisms of disease progression remain poorly understood. Here, we performed unbiased genome-wide CRISPR/Cas9 knockout screens using endocrine sensitive ER+ breast cancer cells to identify novel drivers of resistance to combination endocrine therapy (tamoxifen) and CDK4/6 inhibitor (palbociclib) treatment. Our screens identified the inactivation of JNK signalling, including loss of the kinase MAP2K7, as a key driver of drug insensitivity. We developed multiple CRISPR/Cas9 knockout ER+ breast cancer cell lines (MCF-7 and T-47D) to investigate the effects of MAP2K7 and downstream MAPK8 and MAPK9 loss. MAP2K7 knockout increased metastatic burden in vivo and led to impaired JNK-mediated stress responses, as well as promoting cell survival and reducing senescence entry following endocrine therapy and CDK4/6 inhibitor treatment. Mechanistically, this occurred via loss of the AP-1 transcription factor c-JUN, leading to an attenuated response to combination endocrine therapy plus CDK4/6 inhibition. Furthermore, analysis of clinical datasets found that inactivation of the JNK pathway was associated with increased metastatic burden, and low pJNK activity correlated with a poorer response to systemic endocrine and CDK4/6 inhibitor therapies in both early-stage and metastatic ER+ breast cancer cohorts. Overall, we demonstrate that suppression of JNK signalling enables persistent growth during combined endocrine therapy and CDK4/6 inhibition. Our data provides the pre-clinical rationale to stratify patients based on JNK pathway activity prior to receiving combination endocrine therapy and CDK4/6 inhibition. - Source: PubMed
Publication date: 2025/08/19
Alexandrou SarahLee Christine SFernandez Kristine JWiharja Celine EEshraghi LeilaReeves JohnReed Daniel APortman NeilPhan ZoeMilioli Heloisa HNikolic IvaCadell Antonia LCroucher David RSimpson Kaylene JLim ElgeneHickey Theresa EMillar Ewan K AAlves Carla LDitzel Henrik JCaldon C Elizabeth - The retinal pigment epithelium (RPE) is central to retinal health and immune regulation. In diseases, such as proliferative vitreoretinopathy (PVR), dysregulated RPE function, driven by aberrant signaling pathways like mitogen-activated protein kinase (MAPK), contributes to fibrotic membrane formation and retinal detachment. Tacrolimus, an immunosuppressive agent, has shown potential to modulate signaling beyond immune cells, but its effect on MAPK signaling in RPE cells remains unclear. This study aimed to investigate the impact of tacrolimus on MAPK pathway gene expression and microRNA (miRNA)-mediated regulation in human RPE (H-RPE) cells under inflammatory conditions induced by lipopolysaccharide (LPS). H-RPE cells were treated with LPS and tacrolimus, and cell viability was evaluated by 3- (4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Transcriptomic profiling of 300 MAPK-related genes and corresponding miRNAs was performed using Affymetrix microarrays. Key targets were validated via quantitative reverse-transcription polymerase chain reaction (RT-qPCR) and enzyme-linked immunosorbent assay (ELISA). Gene interaction networks were analyzed with STRING. LPS significantly suppressed MAPK pathway gene and protein expression, including transforming growth factor beta 1 (TGF-β-1), mitogen-activated protein kinase kinase 7 (MAP2K7), mitogen-activated protein kinase 3 (MAPK3), and dual specificity phosphatase 4 (DUSP4). Tacrolimus reversed these effects in a time-dependent manner, restoring expression levels and modulating regulatory miRNAs (e.g., miR-3196, miR-27a/b-3p, miR-190a-3p, miR-149-3p). STRING analysis revealed a highly connected protein network, with MAPK3, MAPK8, and TRAF6 acting as central nodes. Tacrolimus modulates MAPK signaling in H-RPE cells by reversing LPS-induced suppression and regulating specific miRNAs. These findings suggest a potential therapeutic role for tacrolimus in mitigating inflammatory and fibrotic responses associated with PVR. - Source: PubMed
Publication date: 2025/07/01
Kiełbasińska AleksandraKrysik KatarzynaJaniszewska-Bil DominikaMachaj MartynaLelek ZuzannaSzulik MariolaMickiewicz PatrycjaLyssek-Boroń AnitaGrabarek Beniamin Oskar - The stress-responsive kinase MKK7 controls various brain functions. Previously, we showed that neural stem cell-specific deletion of the Mkk7 gene caused abnormal brain development and death immediately after birth (perinatal lethality). However, the region-specific roles of MKK7 during embryonic brain development remain unclear. In this study, we generated three strains of conditional Mkk7 knockout (Mkk7 cKO) mice with deletion of Mkk7 specifically in either the spinal cord, or midbrain/cerebellum, or cerebrum. Loss of MKK7 in the the spinal cord had no effect on mouse embryonic viability, but mice lacking MKK7 in the midbrain/cerebellum displayed perinatal lethality. In contrast, mice with loss of MKK7 in the cerebrum were born at the expected Mendelian ratio but died within five weeks of birth. The brains of these latter mutants showed a thinner cerebral cortex, enlarged ventricles, and decreased phosphorylation of microtubule-associated protein 1B (MAP1B) compared to wild type (WT) brains. This work expands our knowledge of MKK7 functions in the brain and shows that this kinase regulates brain development and maturation in a region-specific manner. - Source: PubMed
Publication date: 2025/07/01
Kofuji SatoshiQian YimingNishina Hiroshi