Ask about this productRelated genes to: MPP3 antibody
- Gene:
- MPP3 NIH gene
- Name:
- membrane palmitoylated protein 3
- Previous symbol:
- DLG3
- Synonyms:
- -
- Chromosome:
- 17q21.31
- Locus Type:
- gene with protein product
- Date approved:
- 1995-05-04
- Date modifiied:
- 2016-10-05
Related products to: MPP3 antibody
Related articles to: MPP3 antibody
- Casein phosphopeptide-amorphous calcium phosphate is a biomimetic remineralizing agent but is unsuitable for individuals with a milk-protein allergy. This exploratory ex vivo study compared low-concentration slurries containing mineralization-promoting peptide-3, sodium fluoride plus mineralization-promoting peptide-3, vehicle cream or casein phosphopeptide-amorphous calcium phosphate on demineralized enamel. - Source: PubMed
Publication date: 2026/08/17
Sahın Rıza MertBal CenkhanMete AyseGungormus MustafaIncıl HilalOrhan Doga EkinKaradas Bakırhan Nurgul - Aging hematopoiesis exhibits progressive myeloid skewing and impaired lymphopoiesis, driving age-related blood disorders. We show that multipotent progenitors (MPPs) mediate this lineage imbalance. Aging expands myeloid-biased MPP3 cells while functionally compromising MPP4 lymphoid potential, collectively skewing hematopoietic output toward the myeloid lineage. We identify Bcl11a as a dosage-sensitive regulator of MPP fate: Bcl11a suppresses Fer to restrain premature myeloid differentiation in MPP3, while activating the Irf8-Ebf1 axis to license lymphoid specification. Strikingly, sustained Bcl11a elevation from development preserves balanced lineage output into old age, reverses age-associated transcriptional alterations, and restores multilineage reconstitution capacity. These findings establish Bcl11a as a key molecular guardian of progenitor integrity during aging and underscore MPPs as a critical cellular nexus where transcriptional control translates into lineage fate decisions. - Source: PubMed
Publication date: 2026/07/20
Zhang LinlinXu XiangWang JingCui XinyuWang CuiYu Yong - Expression of the Csf1r gene in mice is restricted to cells of the mononuclear phagocyte system and placental trophoblasts. A conserved element (Csf1r upstream regulatory element A [CUREA]) in the mouse Csf1r locus contains transcription start sites utilized by trophoblasts and osteoclasts and an enhancer essential for expression of multicopy transgenic reporters in most tissue macrophages. Here, we describe the impact of deletion of CUREA in the mouse genome on the background of a knock-in Csf1r-FusionRed reporter. By contrast to the essential function in transgene expression, CUREA deletion had no effect on expression of FusionRed or differentiation of blood monocytes or tissue resident macrophages. The deletion reduced Csf1r messenger RNA in hematopoietic stem cells and committed myeloid progenitors (MPP3), leading to a subtle differentiation delay, and had a significant impact on microglial density in the brain and the differentiation of osteoclasts. The expression of FusionRed in placenta confirmed expression of CSF1R in trophoblasts. 5'RACE analysis demonstrated that the effect of CUREA deletion on Csf1r transcription in placenta was overcome by the use of cryptic upstream transcription start sites. We conclude that CUREA is a regulatory element controlling Csf1r transcription. The function overlaps with other enhancers identified in the locus and is therefore partly redundant. - Source: PubMed
Maxwell EmmaTaylor IsisFlegg CameronLiu YajunRanpura GinellNooru-Mohamed FathimaGreen Emma KHuang StephenGuo JintaoTeakle NgariSokolowski Kamil AIrvine Katharine MHume David AJacquelin Sebastien - Mutations in the Piezo1 mechanosensor are associated with blood cell anomalies. The objective of our study was to explore the role of Piezo1 in the development and function of the megakaryocyte (MK) lineage. To this end, PF4-Cre mice, bearing Cre recombinase under the control of the gene promoter-which drives expression to hematopoietic progenitors and to the MK/platelet lineage-were crossbred with Piezo1-floxed mice to generate Piezo1 knockout (KO) mice. In our results, the hematopoietic stem cell (HSC) count-including Multipotent Progenitors 2 (MPP2) progenitors that give rise to MKs-tended to be augmented in KO mice, while the level of MPP3 progenitors that give rise to white blood cells (WBCs) tended to be reduced, as compared to matching controls. The level of circulating WBCs was significantly reduced in the KO mice compared to controls. In addition, while platelet count was modestly elevated, platelet activation response was reduced in Piezo1 KO mice compared to controls. MK levels and ploidy were similar in both groups. Baseline serum pro-and anti-inflammatory cytokine profiles were also similar in the two experimental groups. However, upon LPS challenge, there was a significant reduction in IL-6 and INF-γ levels in the sera of Piezo1 KO mice compared to controls. Our findings point to an immunoregulatory and thrombotic potential of Piezo1 in relatively rare bone marrow cells, along with an ability to modulate WBC count. - Source: PubMed
Publication date: 2025/12/16
Singh Shiv VardanKarkempetzaki Anastasia IrisHuang NasiChitalia Vipul CSubramaniam SaravananRavid Katya - Neutropenia is a common complication in oncology patients receiving chemotherapy, and rapid regeneration of functional neutrophils is critical for effective management. Bletilla striata polysaccharide (BSP) has shown therapeutic potential, but its mechanisms and molecular targets remain unclear. Here, we demonstrate that BSP accelerates the recovery of white blood cells, particularly neutrophils, in a chemotherapy-induced neutropenia (CIN) mouse model with cyclophosphamide (CY). The regenerated neutrophils retained phagocytic activity against bacteria, and BSP treatment significantly reduced mortality in the endotoxin-induced mouse death model. Furthermore, BSP enhanced the repopulation of hematopoietic stem and progenitor cells (HSPCs) in the bone marrow and promoted cell-cycle entry, resulting in increased frequencies of long-term hematopoietic stem cells (LT-HSCs), multipotent progenitors 2 (MPP2), and MPP3/4 subsets. Both in vitro colony formation and in vivo competitive transplantation assays confirmed that BSP reshapes hematopoietic reconstitution and corrects aberrant myeloid differentiation. PCR array analysis of HSPCs indicated that this process is mediated by C/EBPε and its downstream genes (LTF, LCN2, and ELANE). Consistently, BSP failed to support myeloid reconstitution following C/EBPε knockdown in vitro. In a C/EBPε knockout mouse model, HSPCs repopulation and regeneration were impaired, and BSP failed to promote neutrophil recovery after CY challenge or the mobilization of MPP2 and MPP3/4 subsets. The regulatory effects of BSP on C/EBPε target genes were also abolished. In conclusion, our findings identify C/EBPε as a key mediator of BSP activity, driving HSPCs repopulation and restoring hematopoietic function. These results highlight BSP as a potential therapeutic strategy for chemotherapy-induced neutropenia. - Source: PubMed
Publication date: 2025/11/28
Cui YaruLuo YingyingZhang ChengShan DanFeng YulinYang ShilinChen LanyingYu Jun