PANX1 Western Blot Kit
- Known as:
- PANX1 Western Blot Kit
- Catalog number:
- ARPK42783_P050
- Product Quantity:
- 25 Western Blots
- Category:
- -
- Supplier:
- ACR
- Gene target:
- PANX1 Western Blot Kit
Related genes to: PANX1 Western Blot Kit
- Gene:
- PANX1 NIH gene
- Name:
- pannexin 1
- Previous symbol:
- -
- Synonyms:
- MRS1, UNQ2529, PX1
- Chromosome:
- 11q21
- Locus Type:
- gene with protein product
- Date approved:
- 2000-07-31
- Date modifiied:
- 2016-10-05
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- Peptide drug discovery for the treatment of chronic kidney disease (CKD) has attracted much attention in recent years due to the urge to find novel drugs and mechanisms to delay the progression of the disease. In this study, we identified a novel short peptide (named YR-7, primary sequence 'YEVEDYR') from the natural Fibroin protein, and demonstrated that it significantly alleviated pathological renal changes in ADR-induced nephropathy. PANX1 was identified as the most notably upregulated component by RNA-sequencing. Further analysis showed that YR-7 alleviated the accumulation of lipid droplets via regulation of the lipid metabolism-related proteins PPAR α and PANK1. Using chemical proteomics, fluorescence polarization, microscale thermophoresis, surface plasmon resonance, and molecular docking, YR-7 was proven to directly bind to β-barrel domains of TGM2 protein to inhibit lipid accumulation. TGM2 knockdown in vivo increased the protein levels of PPAR α and PANK1 while decreased the levels of fibrotic-related proteins to alleviate nephropathy. In vitro, overexpression TGM2 reversed the protective effects of YR-7. Co-immunoprecipitation indicated that TGM2 interacted with PANX1 to promote lipid deposition, and pharmacological inhibition or knockdown of PANX1 decreased the levels of PPAR α and PANK1 induced by ADR. Taken together, our findings revealed that TGM2-PANX1 interaction in promoting lipid deposition may be a new signaling in promoting ADR-induced nephropathy. And a novel natural peptide could ameliorate renal fibrosis through TGM2-PANX1-PPAR α/PANK1 pathway, which highlight the potential of it in the treatment of CKD. - Source: PubMed
Publication date: 2024/05/09
Li Shan-ShanLiu Qiao-JuanBao Jia-XinLu Meng-TingDeng Bing-QuanLi Wen-WenCao Chang-Chun - During cell differentiation, growth, and development, cells can respond to extracellular stimuli through communication channels. Pannexin (Panx) family and connexin (Cx) family are two important types of channel-forming proteins. Panx family contains three members (Panx1-3) and is expressed widely in bone, cartilage and muscle. Although there is no sequence homology between Panx family and Cx family, they exhibit similar configurations and functions. Similar to Cxs, the key roles of Panxs in the maintenance of physiological functions of the musculoskeletal system and disease progression were gradually revealed later. Here, we seek to elucidate the structure of Panxs and their roles in regulating processes such as osteogenesis, chondrogenesis, and muscle growth. We also focus on the comparison between Cx and Panx. As a new key target, Panxs expression imbalance and dysfunction in muscle and the therapeutic potentials of Panxs in joint diseases are also discussed. - Source: PubMed
Publication date: 2024/05/06
Luo YanZheng ShengyuanXiao WenfengZhang HangLi Yusheng - Astrocytes Ca signaling play a central role in the modulation of neuronal function. Activation of metabotropic glutamate receptors (mGluR) by glutamate released during an increase in synaptic activity triggers coordinated Ca signals in astrocytes. Importantly, astrocytes express the Ca-dependent nitric oxide (NO)-synthetizing enzymes eNOS and nNOS, which might contribute to the Ca signals by triggering Ca influx or ATP release through the activation of connexin 43 (Cx43) hemichannels, pannexin-1 (Panx-1) channels or Ca homeostasis modulator 1 (CALHM1) channels. Hence, we aim to evaluate the participation of NO in the astrocytic Ca signaling initiated by stimulation of mGluR in primary cultures of astrocytes from rat brain cortex. - Source: PubMed
Publication date: 2024/04/30
Puebla MarielaMuñoz Manuel FLillo Mauricio AContreras Jorge EFigueroa Xavier F - The channel-forming protein Pannexin1 (Panx1) has been implicated in both human studies and animal models of chronic pain, but the underlying mechanisms remain incompletely understood. - Source: PubMed
Publication date: 2024/04/29
Xing QuCibelli AntonioYang Greta LuyuanDohare PreetiLi Qing-HuaScemes ElianaGuan Fang-XiaSpray David C - Pannexins are large-pore ion channels expressed throughout the mammalian brain that participate in various neuropathologies; however, their physiological roles remain obscure. Here, we report that pannexin1 channels (Panx1) can be synaptically activated under physiological recording conditions in rodent acute hippocampal slices. Specifically, NMDA receptor (NMDAR)-mediated responses at the mossy fiber to CA3 pyramidal cell synapse were followed by a slow postsynaptic inward current that could activate CA3 pyramidal cells but was absent in Panx1 knockout mice. Immunoelectron microscopy revealed that Panx1 was localized near the postsynaptic density. Further, Panx1-mediated currents were potentiated by metabotropic receptors and bidirectionally modulated by burst-timing-dependent plasticity of NMDAR-mediated transmission. Lastly, Panx1 channels were preferentially recruited when NMDAR activation enters a supralinear regime, resulting in temporally delayed burst-firing. Thus, Panx1 can contribute to synaptic amplification and broadening the temporal associativity window for co-activated pyramidal cells, thereby supporting the auto-associative functions of the CA3 region. - Source: PubMed
Publication date: 2024/04/06
Rangel-Sandoval CinthiaSoula MarisolLi Wei-PingCastillo Pablo EHunt David L