Ask about this productRelated genes to: MAP2K2 Blocking Peptide
- Gene:
- MAP2K2 NIH gene
- Name:
- mitogen-activated protein kinase kinase 2
- Previous symbol:
- PRKMK2
- Synonyms:
- MEK2
- Chromosome:
- 19p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1993-11-05
- Date modifiied:
- 2019-04-23
Related products to: MAP2K2 Blocking Peptide
Related articles to: MAP2K2 Blocking Peptide
- Stem cell-derived insulin-producing cells (Ins-PCs) hold great promise for diabetes treatment. Placenta-derived multipotent stem cells (PMSCs) are considered an ideal source of Ins-PC generation due to their immunomodulatory and differentiation properties. However, the cellular and molecular pathways underlying PMSC differentiation to Ins-PCs have not been fully elucidated. In this study, PMSCs were isolated from human placenta and successfully differentiated into Ins-PCs using miRNA-181a mimics. Differentiated Ins-PCs produced a significant amount of insulin and upregulation of C-peptide, insulin, and MAFA expression, compared to undifferentiated control PMSCs. RNA sequencing and LC-MS/MS were performed to uncover the pathways involved in the Ins-PC differentiation process. RNA sequencing revealed the transcriptional landscape of PMSC-derived Ins-PC differentiation. Pathway analysis identified important pathways involved in the differentiation process, including Notch and Wnt/ß-catenin, and so forth. Proteomics analysis further affirmed the presence of key insulin pathway-related proteins involved in the differentiation of PMSCs into Ins-PCs, including LEPR, STC2, MAP2K2, and so forth. Moreover, integrated transcriptomic and proteomic analyses further highlighted LEPR as a potential key regulator for Ins-PC differentiation. These findings demonstrated the feasibility of generating Ins-PCs from PMSCs and identified potential signaling pathways and regulators underlying Ins-PC differentiation, supporting PMSCs as a promising stem cell source of cell-based therapy for diabetes treatment. - Source: PubMed
Publication date: 2026/04/01
Xu JieShen XingguiGu YangLewis David FZoorob DaniWang Yuping - Cardiofaciocutaneous syndrome type 4 (CFC4) is a rare genetic condition caused by pathogenic variants in the MAP2K2 (MEK2) gene, part of the RAS/MAPK signaling pathway. While the broader phenotype of CFC syndrome has been well described, the features specific to this molecular subtype remain poorly defined due to the limited number of cases and underreporting. We conducted a structured analysis of all available literature on CFC4, focusing on organ-specific manifestations, including cardiac, craniofacial, neurological, integumentary, and gastrointestinal features, as well as developmental outcomes, treatment approaches, imaging findings, and behavioral profiles. Cardiofaciocutaneous syndrome type 4 is associated with a recognizable but variable phenotype. Pulmonary valve stenosis and atrial septal defects (ASDs) are the most common cardiac anomalies. Neurological involvement is nearly universal, often presenting as hypotonia and motor delay, with intellectual disability in a subset of cases. Distinctive craniofacial features and ectodermal abnormalities support clinical recognition. Feeding difficulties, sensory integration disorders, and behavioral challenges are frequently observed. Brain magnetic resonance imaging (MRI) abnormalities such as ventriculomegaly and corpus callosum hypoplasia are also relatively frequent. Notably, some individuals with CFC4 exhibit relatively mild phenotypes, with reports of independent functioning in adulthood and a history of familial transmission. In such cases, only mild learning difficulties were described. Better recognition and understanding of CFC4 require consistent and detailed reporting of new cases. To support this, we propose a concise clinical checklist to standardize case descriptions and support diagnosis. - Source: PubMed
Publication date: 2026/03/30
Kubiszewski HubertŚwieca AleksandraŁukasiewicz KacperPierpont Elizabeth IreneSzczałuba Krzysztof - The hypothesis-generating case study aimed at identifying those who are sensitive to anti-PD-L1 and TGF-β bifunctional fusion proteins and exploring potential mechanisms in the treatment of recurrent cervical cancer. We report that recurrent cervical cancer treated with anti-PD-L1 and TGF-β bifunctional fusion proteins in Qilu Hospital of Shandong University show distinct clinical therapeutic outcomes. We describe the clinical course, characteristics, and genetic characteristics of the patients and analyzed the differentially expressed genes (DEGs) following treatment. The elevation of peripheral blood lymphocytes after treatment may predict response to anti-PD-L1 and TGF-β bifunctional fusion proteins, since partial response (PR) and progressive disease (PD) exhibit different trends. A total of 4,844 DEGs were selected between PR and PD patients during the anti-PD-L1 and TGF-β bifunctional fusion protein treatments, which are believed to be involved in the regulation of the immune response. We demonstrated that changing-fate genes continuously change during treatment fostering the IL 17 signaling pathway and TGF-β signaling pathways. Finally, we identified the prognostic genes and validated that high expression levels of PMEPA1, FSTL3, SERPINE1, CXCL1, CXCL8, and low expression levels of JUND，MAP2K2 were significantly associated with poor prognosis of cervical cancer patients using the TCGA database. Anti-PD-L1 and TGF-β bifunctional fusion proteins are feasible and effective for recurrent cervical cancer through the IL 17 signaling pathway and TGF-β signaling pathways. A novel immune infiltration-based gene signature consisting of PMEPA1, FSTL3, SERPINE1, CXCL1, CXCL8, JUND, and MAP2K2 plays a crucial role in recurrent cervical cancer patients with anti-PD-L1 and TGF-β bifunctional fusion proteins. - Source: PubMed
Publication date: 2026/03/23
Mao YucenXing NaidongSun WenxiongBao XinyueLiu XihanWu RichaoPeng Jin - We report a female infant with cardiofaciocutaneous syndrome type 4 (CFC4), an ultra-rare RASopathy caused by a heterozygous (c.619G>A, p.Glu207Lys) variant. From birth, she presented with neonatal hypotonia, respiratory distress, and feeding dysfunction characterized by absent sucking reflex, orofacial hypotonia, and sensory disturbances. Distinct dysmorphic features, including characteristic craniofacial anomalies and macroglossia, were noted. Cardiac evaluation revealed a patent foramen ovale and two small atrial septal defects. Neurologic manifestations included cyanotic apnea, dystonic stiffening, and tremor. Electroencephalography demonstrated bilateral temporoparietal epileptiform discharges, and brain MRI revealed reduced cerebral white matter volume. Although epilepsy has not been definitively diagnosed, the patient remains under ongoing neurological surveillance. Cutaneous involvement included xerotic, papular skin with multiple pigmented nevi and segmental hemangiomas. Ophthalmologic evaluation demonstrated hyperopia with astigmatism. Metabolic assessment suggested mild energetic dysfunction, with elevated triglycerides and citric acid cycle intermediates, without evidence of a defined inborn error of metabolism. Over time, the patient developed persistent feeding difficulties with choking due to oropharyngeal dysfunction, sleep disturbances, delays in gross and fine motor development, and behavioral dysregulation, including aggressive and self-injurious behaviors. Despite the preserved social interest and frequent social approach toward unfamiliar individuals, pronounced anxiety and distress were observed during caregiver absence or reduced attention. This case expands the clinical spectrum of CFC4 associated with MAP2K2 variants, highlighting early feeding dysfunction, paroxysmal neurologic events, and prominent sleep and behavioral disturbances as key diagnostic features. - Source: PubMed
Publication date: 2026/02/11
Świeca AleksandraRydzanicz MałgorzataPloski RafalSzczałuba Krzysztof - The kinase MAPKAPK2 regulates cell survival, proliferation, and death, and is upregulated in colorectal carcinoma (CRC) where it is associated with tumor growth and progression. However, how it regulates tumor progression in conjunction with other signaling pathways, such as MEK/ERK, remains elusive. Solid tumors are often subjected to metabolic stress, notably glucose deprivation. Here, we demonstrate that MAPKAPK2 protein levels in CRC regulate cell fate decision during stress conditions, such as glucose deprivation and therapeutic treatment. While MAPKAPK2 expression is a limiting factor for CRC growth in vitro, depleting MAPKAPK2 or inhibiting its activity pharmacologically provides a survival advantage to CRC cells under glucose limiting conditions. Subjecting CRC cells to low glucose resulted in an ERK1/2-mediated decline in MAPKAPK2 to promote survival. Additionally, cells with reduced MAPKAPK2 activity were less sensitive to trametinib under glucose limiting conditions. Utilizing transcriptomic profiling, we found that glucose deprivation and MAPKAPK2 depletion activate pathways associated with survival during metabolic stress. This relationship was also observed in CRC patients (TCGA), where tumors with low MAPKAPK2 expression had higher ERK1/2 activation and upregulated stress-induced pathways, leading to poor survival. Finally, MAPKAPK2 modulated growth of CRC organoids, subcutaneous tumors, and patient-derived xenografts (PDX), and reduced MAPKAPK2 levels decreased efficacy of trametinib, in vitro and in vivo. Overall, this study identifies an interrelationship between MEK/ERK and p38/MAPKAPK2 signaling pathways during glucose deprivation to support cell survival and features MAPKAPK2 loss as a possible mechanism leading to reduced efficacy of trametinib-based anticancer therapy and poor patient outcomes in CRC. - Source: PubMed
Publication date: 2026/02/09
Kumari NitiChen XuBaldwin Amber MClemons Kristin IEl-Harakeh MohammadCalisto Lilian EKumar BalawantZhang QiaoqiaoMin JiangXiao BinSingh Amar BWang BinNorth Brian J