Recombinant Human PDCD4
- Known as:
- Recombinant Human PDCD4
- Catalog number:
- CF62
- Product Quantity:
- 10ug
- Category:
- -
- Supplier:
- Novoprotein
- Gene target:
- Recombinant Human PDCD4
Related genes to: Recombinant Human PDCD4
- Gene:
- PDCD4 NIH gene
- Name:
- programmed cell death 4
- Previous symbol:
- -
- Synonyms:
- H731
- Chromosome:
- 10q25.2
- Locus Type:
- gene with protein product
- Date approved:
- 2000-05-10
- Date modifiied:
- 2016-11-30
Related products to: Recombinant Human PDCD4
Related articles to: Recombinant Human PDCD4
- Periodontitis is a chronic inflammatory disease characterized by progressive alveolar bone destruction and represents a major cause of tooth loss. It has also been associated with systemic inflammatory conditions such as diabetes. Circadian rhythms, governed by clock genes, are essential for maintaining physiological homeostasis across various tissues. Circadian rhythm disruption, such as that caused by night shift work, has been associated with severe periodontitis; however, the underlying mechanisms remain incompletely understood. Period 2 (Per2), a core peripheral clock gene expressed in periodontal tissues, was investigated for its role in inflammatory bone loss under circadian disruption. In a murine ligature model, circadian disruption exacerbated alveolar bone loss, while Per2 deficiency amplified inflammatory responses. Consistently, PER2 knockdown in TNF-α-stimulated human periodontal ligament cells (hPDLCs) led to increased expression of pro-inflammatory cytokines IL-1β and IL-6. Interestingly, Per2 knockout also led to increased basal bone mass compared with wild-type mice. Mechanistically, we found miR-21, a PER2-regulated microRNA, displayed rhythmic expression in hPDLCs and was downregulated following PER2 knockdown. Further investigation demonstrated that the PER2/miR-21 axis negatively regulates osteogenic differentiation under non-inflammatory conditions via TGF-β/SMAD signaling, while under inflammatory conditions, its downregulation failed to suppress PDCD4/NF-κB signaling, resulting in elevated pro-inflammatory cytokine secretion. Finally, local delivery of miR-21 agomir significantly promoted bone recovery after ligature removal. Together, these findings identify PER2 as a key circadian regulator of inflammation-associated bone homeostasis and highlight miR-21 as a potential therapeutic target for bone regeneration in periodontitis. - Source: PubMed
Publication date: 2026/05/22
Li ShiyuZhu JingxianLiu NiankeWang XinLi YangChen QingYin WeiSong Yaling - Platelet-derived microRNAs (miRNAs) are regarded as diagnostic biomarkers as well as potent regulators of cancer development. The expression of miR-21, a vital miRNA, is elevated in the tumor tissues of osteosarcoma (OS) patients. However, platelet-derived miR-21 in OS is unknown. Here, we found that the level of miR-21 is increased in the serum of OS patients. The miR-21 level is associated with advanced tumor stages and poorer clinical outcomes in OS patients. Moreover, platelet-derived microvesicles (PMVs) from OS patients (OS-PMVs) significantly enhanced the miR-21 profile in MG63 OS cells. Functional assays revealed that the proliferation and migration of MG63 cells were promoted by OS-PMV incubation or the transfection of miR-21 mimics, whereas the sensitivity of MG63 cells to methotrexate (MTX), doxorubicin (ADM), and cisplatin (DDP) was reduced. However, inhibiting miR-21 partially reversed the OS-PMV-mediated effects. Furthermore, programmed cell death 4 (PDCD4) was identified as a potential target of miR-21 in OS. miR-21 considerably inhibited PDCD4 expression in MG63 cells and reversed the antitumor effects mediated by PDCD4 overexpression. In conclusion, our results suggest that platelet-rich miR-21 may promote the development of OS by targeting PDCD4. - Source: PubMed
Pan Xi'anDong ShishiSun FaruiZhang YuanjinZhang GuofuLi JunLiu Bingxia - MicroRNAs (miRNAs) are short RNA molecules that bind to target mRNAs, resulting in translational repression and gene silencing. Overexpression of microRNA-21 (miR-21) is associated with various human diseases, including autosomal dominant polycystic kidney disease (ADPKD) and pulmonary fibrosis. In this study, a previously described heterobifunctional molecule, TGP-21-RiboTAC, that degrades the miR-21 precursor (pre-miR-21) in triple-negative breast cancer cells was investigated in polycystic kidney cell lines and a lung fibroblast cell line. In the former, TGP-21-RiboTAC degraded pre-miR-21 and derepressed miR-21's downstream targets, programmed cell death 4 (PDCD4) and peroxisome proliferator-activated receptor alpha (PPARα), known drivers of ADPKD. The heterobifunctional molecule also inhibited cyst growth and rescued the metabolic alterations that occur in ADPKD. In the lung fibroblast cell line, MRC-5, TGP-21-RiboTAC also reduced pre- and mature miR-21 levels, rescued transforming growth factor β (TGF-β)-induced repression of SMAD family member 7 (SMAD7), and inhibited cell invasion. Collectively, these studies demonstrate the potential of targeted RNA degradation as therapeutic agents that retard the development of organ fibrosis. - Source: PubMed
Publication date: 2026/05/18
Wang TenghuiYang XueyiLee YeongjuSong Jin HChilds-Disney Jessica LGarcia Joe G NDisney Matthew D - Betulinic acid is defined as a hydrophobic pentacyclic triterpenoid primarily found in the bark of Betula alba, known for its anticancer activity through mechanisms such as upregulating proapoptotic proteins, modulating NF-kB, and inhibiting topoisomerase I. The current study aimed to explore the anticancer potential effect, molecular targets, and association with miR-21 modulation after BA treatment and its combination with doxorubicin against human triple-negative breast cancer (MDA-MB-231) cells. We determined drug cytotoxicity by MTT assay, and death mechanism by flow cytometry. Besides, the potential effect of BA and DOX treatment on downstream effect of miR-21 on HIF1A, PDCD4, PTEN and SMAD7 expression levels. Finally, a molecular docking study was performed to determine molecular targets, binding affinity, and mode of interactions of BA and DOX with HIF1A, PDCD4, PTEN and SMAD7. Collectively, our data showed that treatment with BA and/or DOX have significantly describing observed differences under the tested conditions associated with increasing apoptosis, downregulation of miR-21, HIF1A and SMAD7 expression and upregulation of PDCD4 and PTEN. Finally, the molecular docking study suggested potential interactions between BA and DOX with PTEN and PDCD4, modulating their activities leading to growth arrest and cell death. In conclusion, this study reported BA as potential antiproliferative compound with modulation of miR-21 expression and identified molecular targets involved in its action. - Source: PubMed
Publication date: 2026/05/16
Mahmoud Mohammad AAbdo HagarMekky MariamSalem TasneemMabrouk SaraKhaled Basmala - Non-coding RNAs (ncRNAs) influence gene expression and diverse physiological and pathological processes. Long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) play roles in cancer and neurodegenerative diseases. LncRNAs, such as HOTAIR, MALAT1, and NEAT1, regulate chromatin remodeling through histone modification. Dysregulated expression leads to oncogenesis and neuronal dysfunction. Conversely, miRNAs such as miR-21 and miR-155, as post-transcriptional regulators, act in oncogenic signaling and neuroinflammation. MiR-21 targets PTEN and PDCD4, leading to aberrant activation of the PI3K/AKT and NF-κB pathways, thereby promoting cancer cell proliferation, while influencing neuronal apoptosis and neuroprotection. Similarly, miR-155 modulates SHIP1 and SOCS1 through AKT and JAK/STAT pathways in both cancer and neurodegenerative contexts. The convergence of these signaling cascades reveals a shared molecular framework that links tumor progression to neurodegeneration. Understanding the intricate lncRNA-miRNA-mRNA regulatory networks provide valuable insights into disease mechanisms and clinical applications regarding ncRNAs as biomarkers. Further research integrating transcriptomics, functional genomics, and therapeutic delivery systems is essential to harness the full diagnostic and therapeutic potential of ncRNAs. - Source: PubMed
Publication date: 2026/05/16
Das AnanyaBhuiyan Afsana