MKK3 Recombinant Adenovirus
- Known as:
- MKK3 Recombinant Adenovirus
- Catalog number:
- ADV-120
- Product Quantity:
- 50
- Category:
- -
- Supplier:
- Cell Biolabs
- Gene target:
- MKK3 Recombinant Adenovirus
Related genes to: MKK3 Recombinant Adenovirus
- Gene:
- MAP2K3 NIH gene
- Name:
- mitogen-activated protein kinase kinase 3
- Previous symbol:
- PRKMK3
- Synonyms:
- MEK3, MKK3, MAPKK3
- Chromosome:
- 17p11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1997-11-11
- Date modifiied:
- 2016-10-05
Related products to: MKK3 Recombinant Adenovirus
Related articles to: MKK3 Recombinant Adenovirus
- Distinguishing whether genetic variants in protein kinases cause gain or loss of function is critical in clinical genetics. In particular, gain (and not loss)-of-function variants are often immediately amenable to treatment by inhibitors, making their identification a potential boon to personalised medicine. Most existing computational methods for variant pathogenicity prediction simply distinguish damaging from benign variants and provide no further functional insights. Here, we present a data-driven approach that differentiates activating, deactivating, and resistance variants. - Source: PubMed
Publication date: 2025/10/28
Singh GurdeepSchmenger TorstenGonzalez-Sanchez Juan CarlosKutkina AnastasiiaBremec NinaDiwan Gaurav DMozas PabloLópez CristinaSiebert ReinerSotillo RocioRussell Robert B - Bone marrow-derived mesenchymal stromal cells (BMSCs) are multipotent cells that have attracted considerable attention in regenerative medicine. Current in vitro test focus on biochemical assays of hair cell-like cells (HCLCs) derived from BMSCs associated with changes in electrophysiological properties. HCLCs were produced from BMSCs by culturing BMSCs with B27, EGF, FGF, and IGF-1. RNA Sequencing studies, immunocytochemistry (ICC) and double immunofluorescence staining were used to test hair cell-associated markers on day 17 and 21-26. Next, we performed whole-cell patch-clamp recording by utilizing current- and voltage-clamp techniques to assess changes in membrane potential and ionic currents during differentiation. Immunostaining assay reveals significant expression of myosin VIIA and SOX2 in cultured hair cells on day 21-26. We have also found 8 enhanced transcripts in differentiated cell genes (Wnt7a, Mgat5b, Myo7a, Pou4f3, SOX2, Atoh1, Map2k3, Actin) using RNA Sequencing. Electrophysiological results indicate that cells undergoing differentiation had an average resting membrane potential (RMP) of -11.93 ± 0.89 mV on day 17 and -58.96 ± 1.10 mV on days 21-26. Differentiated HCLCs displayed a mean resting membrane resistance of 171.66 ± 29.12 MΩ, membrane time constant of 10.73 ± 0.45 ms and membrane capacitance of 0.0625 ± 0.0087 pF, following 21-26 days in culture. Our results also showed cultured HCLCs express transcriptomic profile of this cell type. These findings indicate that alterations in RMP may serve as a valuable indicator for distinguishing HCLCs differentiation potential from BMSCs. - Source: PubMed
Publication date: 2025/09/26
Peyvandi Ali AsgharDavoudi ShimaBazgir NargesJanahmadi MahyarNorioun HamidKhoshsirat ShahrokhNiknazar Somayeh - Colorectal cancer (CRC) remains a leading cause of cancer-related deaths, with notable sex-specific differences in its incidence, diagnosis, and outcomes. Our previous work identified casein kinase 2 alpha (CK2α) as being capable of impairing DNA mismatch repair (MMR) via phosphorylation of MLH1, thereby increasing the tumor mutational burden. This study aimed to investigate sex-specific differences in CK2α protein expression in CRC. - Source: PubMed
Publication date: 2025/08/30
Friedrich Jana RomyMeier ClaraPlotz GuidoZeuzem StefanBrieger AngelaOverby Sarah J - Pancreatic ductal adenocarcinoma (PDA) remains one of the most lethal malignancies with limited early diagnostic and therapeutic options. Although receptor for activated C kinase 1 (RACK1) is an evolutionarily conserved scaffold protein, its functional role and mechanistic involvement in PDA pathogenesis remain elusive. - Source: PubMed
Publication date: 2025/09/01
Zhang WeiJiang TingtingZhang HuiqingWei FangLi XiaojiaXie Keping - Obesity, a major risk factor for osteoarthritis (OA), is related to increased circulating levels of free fatty acids (FFAs). However, the molecular mechanism underlying this metabolic OA phenotype remains unknown. We found that mice fed a high-fat diet (HFD) became obese and developed OA in their knee joints. Macroautophagy/autophagy activity was significantly reduced in articular cartilage of mice fed an HFD or in chondrocytes exposed to FFAs. Using conditional knockout (cKO) mice with cartilage-specific deletion of to inhibit autophagy and sh-lentiviral-transduced chondrocytes in , we showed that autophagy deficiency aggravated HFD-induced OA progression and chondrocyte extracellular matrix (ECM) degradation. Mechanistically, STING1 was degraded in an autophagy-dependent manner. Autophagy deficiency increased STING1 levels, in turn activating the STING1-TBK1-IRF3 and MAP2K3/MKK3-MAPK/p38 signaling pathways, thereby triggering cartilage ECM degradation. These findings suggested that the HFD-autophagy-STING1 axis played a pivotal role in OA development, providing a potential therapeutic strategy for obesity-associated OA.: 3-MA: 3-methyladenine; ACAN: aggrecan; AOD: average optical density; ATG7: autophagy related 7; BafA1: bafilomycin A1; CGAS: cyclic GMP-AMP synthase; cKO: conditional knockout; COL2A1: collagen, type II, alpha 1; DMM: destabilizing the medial meniscus; DMXAA: 5. - Source: PubMed
Publication date: 2025/08/06
Kang XiaominLiu WenjuanMa XiaoFeng DongxuSun HongzhiWu Shufang