Ask about this productRelated genes to: PROM2 antibody
- Gene:
- PROM2 NIH gene
- Name:
- prominin 2
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 2q11.1
- Locus Type:
- gene with protein product
- Date approved:
- 2003-03-25
- Date modifiied:
- 2015-08-25
Related products to: PROM2 antibody
Related articles to: PROM2 antibody
- Research has indicated a connection between pyroptosis and psoriasis, yet the specific genes involved remain largely unidentified. This study employed Mendelian randomization (MR) to evaluate the potential causal impact of both pyroptosis-related genes and DNA methylation signatures on psoriasis risk. - Source: PubMed
Publication date: 2026/03/12
Dong WenwuShi Cuiping - Environmental changes in rivers caused by fluctuations in water temperature and increasingly intense rainfall linked to climate change are likely to influence the physiological condition (environmental stress) of wild Japanese eels (). This study examined the epidermal mucus of , which can be collected noninvasively in the field, and evaluated whether RNA-Seq analysis could characterize the physiological state of this species in response to such environmental stressors. We conducted controlled tank trials simulating (1) suspended solids (SS) stress resulting from sediment runoff during heavy rainfall (using kaolin clay addition) and (2) water temperature variations (10 °C, 20 °C, and 30 °C) as physical stresses experienced by wild under climate-driven changes. Subsequently, we performed RNA-Seq analysis to determine genes in the epidermal mucus responsive to each experimental stressor. As a result, under (1) SS stress, genes associated primarily with cellular immunity and inflammatory pathways showed elevated expression. In the (2) water temperature trials, relative to the control (20 °C), the low-temperature group (10 °C) displayed increased expression of lipid-metabolism-related genes such as , , and , whereas the high-temperature group (30 °C) exhibited heightened expression of genes linked to the heat-shock response. Thus, because this study enabled the identification of genes specifically expressed in reaction to each stressor from the epidermal mucus of , these findings are expected to support the future development of noninvasive approaches for evaluating the physiological state (health condition) of wild . - Source: PubMed
Publication date: 2026/03/09
Yasuike MotoshigeAsakura TaigaNakamura YojiHongo YukiFukuda Nobuto - Osteoarthritis (OA) remains a debilitating joint disorder due to the lack of disease-modifying therapies that can simultaneously halt cartilage degradation and modulate the aberrant immune microenvironment. This study demonstrated the therapeutic potential of extracellular vesicles derived from adipose-derived stem cells preconditioned with nanosecond pulsed electric fields (NsPEFs-ADSCs-EVs). Administration of NsPEFs-ADSCs-EVs significantly attenuated OA progression, as indicated by alleviated cartilage degradation, and a marked shift in synovial macrophage from the pro-inflammatory M1 to the pro-reparative M2 phenotype. Mechanistically, we discovered that NsPEFs-ADSCs-EVs, via surface-enriched ITGA4, activated the PI3K/Akt pathway to instruct the increased secretion of R-spondin 3 (RSPO3). We further unveiled a novel dual function of chondrocyte-derived RSPO3. It acted in an autocrine manner to enhance chondrocyte anabolism and in a paracrine manner to directly drive M2 macrophage polarization. The pro-M2 effect was specifically mediated through the activation of the LGR4/LRP6/β-catenin signaling axis in macrophages. Collectively, this work elucidates a previously unrecognized paracrine axis wherein NsPEFs-engineered EVs deploy RSPO3 as a significant coordinator to synchronously promote cartilage regeneration and immune resolution. Our findings not only reveal RSPO3 as a promising therapeutic target but also establish the NsPEFs platform as a efficient strategy for generating functionally enhanced EVs, offering a novel cell-free strategy for OA therapy. - Source: PubMed
Publication date: 2026/01/17
Wang YushanGao YingjieCao ZhiyanDong MingjieShao PengfeiFan HaoGuo ZijianHu XiaoyongCheng WenxiangLi PengcuiZhang WeiFeng YiFu PanfengGe ZigangXu JiakeXiang Chuan - This study aimed to investigate the prognostic value and biological implications of cuproptosis/ferroptosis-related genes in breast cancer, and to develop a robust molecular signature for risk stratification and treatment guidance. - Source: PubMed
Publication date: 2025/11/17
Wei YuqinWei XingwenZhao Wei - Macrophage M2 polarization plays a pivotal role in breast cancer development. The present study aimed to investigate the interplay of the Leupaxin (LPXN)/HDAC6/EGR2 axis in breast cancer and its impact on macrophage M2 polarization. Our findings indicate that LPXN overexpression in breast cancer tissues correlates with M2 macrophage polarization. To investigate LPXN's potential role, we conducted siRNA-mediated silencing in macrophages. In a breast cancer cell-macrophage co-culture system, LPXN silencing was associated with reduced cancer cell proliferation, decreased M2 polarization markers, and diminished HDAC6 expression. BIOGRD and experimental data suggest a regulatory relationship between LPXN and HDAC6. Notably, HDAC6 inhibition partially reversed the pro-M2 effects of LPXN overexpression. Further mechanistic studies revealed that HDAC6 interacts with EGR2, functioning as its deacetylase and negatively regulating EGR2 expression. EGR2 silencing partially attenuated the anti-M2 effects observed with LPXN knockdown. In murine breast cancer models, LPXN silencing was linked to increased M1 macrophage markers and reduced tumor burden. These findings suggest LPXN may influence breast cancer progression through HDAC6/EGR2-mediated regulation of macrophage polarization. In conclusion, our study demonstrated that the LPXN/HDAC6/EGR2 axis promotes breast cancer progression by augmenting macrophage M2 polarization. - Source: PubMed
Publication date: 2025/11/25
He ShaozhongWang QunHe JiayiChen ZhongyongXiao Yumei