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
- Patients with advanced biliary tract cancers (aBTC) are in urgent need of additional/new treatment options. We aimed to assess the efficacy and safety of ivonescimab plus chemotherapy in patients with aBTC. - Source: PubMed
Publication date: 2026/07/06
Xu QiZhou ShuruiZhang ChenboZhou YiwenHe YatongJiang YvchaoLi JingjingYi TienanLuo CongZhang LeiWu JiaZhang YuhuaWu MinhuaWei QingLi QiLiu BoChen XiangmingYao YinyeYu ChengkunLi JijuanRen YanZhuo WeiYuan LiLi WentingWang Zhongmin MaxwellLi BaiyongXia MichelleXie YanruWu KuiYing Jieer - Breast cancer remains one of the most prevalent malignancies among women, with doxorubicin resistance posing a significant challenge that undermines treatment success and survival outcomes. Aberrant alternative splicing (AS), driven by dysregulation or mutations in splicing factors (SFs), is implicated in cancer initiation, progression, and drug resistance. This study aims to investigate the association of the epithelial cell-specific splicing factor ESRP1 with doxorubicin resistance in breast cancer, focusing on how ESRP1 deficiency correlates with AS changes that promote chemoresistance. - Source: PubMed
Publication date: 2026/06/21
Zhang JingChen LibinSong QinglingXu LiLi YinghuaLi WenWang Jie - The c-Jun N-terminal kinase (JNK) pathway is a central driver of fibrosis, inflammation, and neurodegeneration. While direct JNK inhibitors have shown therapeutic promise, achieving high isoform selectivity remains a significant medicinal chemistry challenge. Furthermore, targeting the upstream 'gatekeepers' MKK4 and MKK7 offers a distinct mechanism to modulate pathway output with greater precision. Consequently, medicinal chemistry efforts have shifted upstream to the dual-specificity kinases MKK4 and MKK7. This review critically evaluates the structural biology and pharmacological evolution of small-molecule inhibitors targeting these nodes. We contrast the distinct therapeutic landscapes of the two kinases: while MKK4 inhibition has emerged as a breakthrough strategy for unlocking liver regeneration (exemplified by the first-in-class clinical candidate HRX215), MKK7 inhibition is primarily pursued for its anti-fibrotic and anti-inflammatory potential. Special attention is given to structure-based design strategies, including the exploitation of the unique hinge-region cysteine (Cys218) for MKK7-specific covalent targeting and the optimization of scaffold selectivity against off-targets like BRAF. Finally, we discuss emerging modalities, such as PROTACs and dual inhibitors, outlining a roadmap for the next generation of precision therapeutics targeting the MKK-JNK axis. - Source: PubMed
Publication date: 2026/02/15
Zhao MinLi BaojianGao YingLiang YanShao NanqiShi XinboLi Jie - The development of anti-inflammatory drugs is a research focus. Acute lung injury (ALI) is a life-threatening inflammatory syndrome that currently lacks effective pharmacotherapies. Here, we report a potential therapy for ALI by targeting c-Jun N-terminal kinase 2 (JNK2), a key regulator of MAPK pathway-driven inflammatory responses. Through structure-based virtual screening and systematic structural optimization, we identified compound , which potently inhibited the secretion of IL-6 in THP-1 (IC = 0.14 μM) and TNF-α in J774A cells (IC = 0.55 μM). Mechanistic studies revealed that functioned through the dual inhibition of JNK2 kinase activity and the protein-protein interaction between MKK7 and JNK2, thus inhibiting the phosphorylation of c-Jun and thereby attenuating the LPS-induced inflammatory cytokine overexpression. Furthermore, showed potent therapeutic effects on both LPS- and CLP-induced ALI in mice and exhibited favorable pharmacokinetics and safety profiles, establishing as a promising candidate for ALI treatment. - Source: PubMed
Publication date: 2026/02/23
Chen QiDong KeZhan YapingHuang NanChen PanJiang MiaoZhu LuxiaoZhang KaixinLv YuehuaZou YuChen ZhichaoGuo MiSun ChenhuiCho Young-ChangZeng RuifengWu DiLiang GuangTang Qidong - This study investigated whether alterations in the expression of genes integral to the c-Jun N-terminal kinase (JNK) signaling pathway play a role in the pathogenesis of colorectal cancer (CRC). It analyzed the expression of genes encoding two JNK isoforms (MAPK8 and MAPK9) and the JNK-activating kinases (MAP2K4 and MAP2K7). Gene expression patterns in CRC tissue were compared with existing data in public online databases to provide an integrated understanding of their potential role in tumorigenesis. The material consisted of 55 cancer tissue fragments collected intraoperatively from patients with histopathologically confirmed CRC. Total RNA isolated from these tissues was used to determine the relative expression of the selected genes using quantitative PCR. Additionally, data from publicly accessible bioinformatics databases were utilized. gene expression was significantly elevated in tumor specimens with higher histological grades. Conversely, gene expression tended to be higher in tumor tissues with lower histological grades. Moreover, elevated MAPK8 gene expression was linked to an increased incidence of regional lymph node metastasis. Furthermore, bioinformatics analysis confirmed that and appear to promote tumor aggressiveness and metastasis, whereas and may have a protective or regulatory role in early stages of the disease. - Source: PubMed
Publication date: 2025/12/22
Wosiak AgnieszkaWodziński DamianŚwiechowski RafałPietrzak JacekMik MichałBalcerczak Ewa