MEIS2 Mouse Monoclonal Antibody
- Known as:
- MEIS2 Mouse Monoclonal Antibody
- Catalog number:
- BIN-004212-M01
- Product Quantity:
- 0.1mg
- Category:
- -
- Supplier:
- Zyagen
- Gene target:
- MEIS2 Mouse Monoclonal Antibody
Related genes to: MEIS2 Mouse Monoclonal Antibody
- Gene:
- MEIS2 NIH gene
- Name:
- Meis homeobox 2
- Previous symbol:
- -
- Synonyms:
- MRG1, HsT18361
- Chromosome:
- 15q14
- Locus Type:
- gene with protein product
- Date approved:
- 1998-02-09
- Date modifiied:
- 2014-11-19
Related products to: MEIS2 Mouse Monoclonal Antibody
Related articles to: MEIS2 Mouse Monoclonal Antibody
- : MEIS proteins are essential homeobox transcription factors that play critical roles in development and have been increasingly implicated in oncogenesis, including breast cancer. : In this study, we identified and characterized novel small-molecule MEIS2 inhibitors through in silico docking targeting the active region of the human MEIS2 homeobox domain. Lead candidates MEISi-2E, MEISi-3, and MEISi-4 were identified with binding energies ranging from -3.0 to -3.90 kcal/mol. The inhibitory potential of these molecules was validated in vitro using a species-conserved MEIS-Luciferase Reporter construct containing the TGACAG targeted locus. : Our results demonstrate that MEISi-2E, MEISi-3, and MEISi-4 significantly suppress MEIS-driven luciferase activity and downregulate the expression of , , and downstream genes such as , , , , and while upregulating negative regulator and . In breast cancer cell lines, these inhibitors exhibited potent growth inhibition, with MEISi-3 showing an exceptional IC50 as low as 0.1 μM in SK-BR-3 cells. Mechanistic studies using flow cytometry revealed that these inhibitors induce dose-dependent apoptosis and necrosis. Importantly, the novel inhibitors showed minimal toxicity to healthy human dermal and MRC5 fibroblasts, suggesting a favorable safety profile. : These findings establish these small molecules as promising therapeutic candidates for targeting MEIS2-dependent pathways in breast cancer. - Source: PubMed
Publication date: 2026/06/01
Kocabaş FatihGirgin BirkanUslu MerveSiyah PınarMermer Arif - The frontal lobe comprises the prefrontal association cortex (PFC), which supports complex cognition and goal-directed behavior, and the motor cortex (MC), which executes movement. A hallmark of primate brain evolution is PFC expansion accompanied by a posterior displacement of the MC. Retinoic acid (RA) signaling has emerged as a key regulator of PFC specification and expansion. However, the mechanisms that spatially confine RA signaling within the developing PFC, and the downstream RA-responsive gene networks, remain poorly understood. Here we defined an RA-associated gene regulatory network (RA-GRN) in the developing human PFC and identified , which encodes a transcription factor linked to intellectual disability and autism spectrum disorder (ASD), as its key hub of this network. Conditional deletion of in postmitotic cortical excitatory neurons in mice results in a partial respecification of prospective prefrontal association territories toward motor-like molecular and connectional features, highlighting a critical role of postmitotic neurons in establishing and maintaining cortical areal identities. Concomitant with loss, the population of excitatory neurons expressing the RA-synthesizing enzyme ALDH1A3, and consequently RA signaling itself, is markedly reduced in the developing medial prefrontal cortex (mPFC). These findings revealed a conserved autoregulatory loop: RA → MEIS2 → ALDH1A3 → RA that reinforces a PFC-enriched RA gradient and organizes the MC-PFC axis. Together, our findings reveal a postmitotic mechanism by which specific features of neuronal identity reinforce RA signaling to define key features of prefrontal and motor cortical territories, linking a classic morphogen to transcriptional identity, neural circuit formation and function, and potentially to psychiatric disorders. - Source: PubMed
Publication date: 2025/12/25
Yang LinShibata MikihitoPark SaejeongLiu YutingSalamon IvaLiu JiaKim Suel-KeeShibata AkemiDeveau-French AshleyMato Blanco XoelBai SuxiaNottoli TimothyXing XiaojunRohani NarjesSanders Stephan JKovner RothemPattabiraman KartikSestan Nenad - The vomeronasal organ (VNO) is a specialized chemosensory structure that detects chemical cues involved in predator avoidance, social interactions and reproductive behaviors. In mice, the VNO contains distinct vomeronasal sensory neurons (VSNs) that express vomeronasal receptors (VRs) and formyl peptide receptors. Apical VSNs express Meis2, V1Rs and Gαi2, whereas basal VSNs express Tfap2e (also known as AP-2ε), V2Rs and Gαo. Type 2 VRs (V2Rs) are classified into families A-E, and basal neurons co-express a family C receptor with a VR from another family. Single-cell RNA-sequencing identified ∼980 genes differentially expressed between V1R- and V2R-expressing neurons, many of which are linked to endoplasmic reticulum (ER) functions. Notably, canopy 1 (Cnpy1) is highly enriched in V2R-expressing neurons. The VNO of Cnpy1 knockout mice develops normally but undergoes progressive loss of V2R-expressing neurons, which is associated with increased ER stress gene expression, upregulation of family C V2R mRNAs and reduced V2R protein levels. V2R-expressing VSNs in Cnpy1 knockouts fail to respond to pheromones, show altered guidance and adhesion gene expression, and display disrupted connectivity with the accessory olfactory bulb. These findings emphasize the role of cell-specific ER protein repertoires in maintaining neuronal function. - Source: PubMed
Publication date: 2026/06/19
Mathias Nicholas ADolphin Nikki MLeFever Noah MAmato EnricoYbanez Carlsy SRuquet AnthonyForni Paolo E - Neurogenesis takes place in the subventricular zone (SVZ) and in the dentate gyrus (DG) of the hippocampus of many adult mammalian species. Recent findings indicate that calpain-2 could participate in neurogenesis regulation through the truncation of the transcription factor, Myeloid Ecotropic Viral Integration Site 2 (MEIS2). The present study aimed to test the effects of calpain-2 inhibition/deletion on MEIS2 levels and neurogenesis in adult mice. - Source: PubMed
Publication date: 2026/06/09
Baudry MichelReece TristanShahi RoxanaTa KatelynBi Xiaoning - Metabolic dysfunction contributes to the risk and progression of Alzheimer's disease (AD), yet the cellular mechanisms linking impaired insulin signaling and systemic metabolic stress to brain dysfunction remain incompletely defined. - Source: PubMed
Publication date: 2026/06/03
Nicholson LaShaeTang Si JieKarra TejaswiniAbouelatta HabibaStrittmatter Stephen M