Ask about this productRelated genes to: MPZL1 antibody
- Gene:
- MPZL1 NIH gene
- Name:
- myelin protein zero like 1
- Previous symbol:
- -
- Synonyms:
- PZR, FLJ21047
- Chromosome:
- 1q24.2
- Locus Type:
- gene with protein product
- Date approved:
- 1999-06-14
- Date modifiied:
- 2016-01-19
Related products to: MPZL1 antibody
Related articles to: MPZL1 antibody
- While anti-CD20 antibodies like obinutuzumab (OBI) have improved clinical outcomes, B-cell malignancies remain a significant therapeutic challenge. OBI induces direct cell death (DCD) and augments antibody-dependent cellular cytotoxicity (ADCC), but the molecular mechanisms involved in DCD remain unclear. This study aims to bridge this knowledge gap and develop enhanced treatment modalities. - Source: PubMed
Publication date: 2026/04/15
Choi A-YeonKim DaHyeLee ChangsinAhn Jae-SookYang Deok-HwanLee DongHyukKim Joo Young - Triple-negative breast cancer (TNBC) is an aggressive subtype of breast cancer with limited therapeutic treatments. This study evaluates the anticancer activity and mode of action of the copper(II) complex [Cu(HL)(NO)HO]·HO (CuHL), derived from (E)-N'-(2-hydroxy-3-methoxybenzylidene)furan-2-carbohydrazide (HL), against a panel of TNBC cell lines (MDA-MB-231, MDA-MB-468, MDA-MB-157, HCC1806). CuHL exhibits potent cytotoxicity in the low micromolar range (IC ≈ 2 µM), surpassing cisplatin by up to 81-fold. In MDA-MB-231 cells, CuHL inhibits colony formation and induced reactive oxygen species (ROS) generation in a concentration-dependent manner. Moreover, CuHL triggers apoptosis as evidenced by Annexin V/PI staining and the modulation of Bax, Bcl-2, caspase-3, and cleaved caspase-3 protein levels. Label-free quantitative proteomics reveal 34 differentially expressed proteins, implicating pathways related to heat shock response, protein folding, lipid metabolism, and cell migration. Notably, CuHL downregulates BCAR3, AJUBA, MPZL1, TP53, FASN, and HMGCS1, suggesting inhibition of prometastatic and lipid biosynthetic processes. Functional assays confirm reduced migratory capacity in MDA-MB-231 cells. These findings position CuHL as a promising candidate for TNBC therapy, meriting further in vivo evaluation. - Source: PubMed
Santa Maria de la Parra LucíaMartínez Valeria RNayeem NaziaContel MariaLeón Ignacio E - Sepsis is a Systemic Inflammatory Response (SIR) caused by invading pathogens. We aimed to characterize infiltrating cells in sepsis and provide novel insight for the treatment of sepsis. - Source: PubMed
Liu LiyaoZhao LinTan Jixiang - Protein Zero Related (PZR) is a type I transmembrane glycoprotein encoded by the MPZL1 gene and a member of the immunoglobulin superfamily (IgSF). Despite sharing 46 % sequence homology in its extracellular domain with myelin P0 protein (MPZ), PZR exhibits distinct functional specialization. It undergoes alternative splicing to generate three isoforms (PZR, PZRa, PZRb) with tissue-specific expression patterns, predominantly enriched in cardiovascular, renal, and pancreatic tissues, and localized to cell-cell contact sites and migration-associated domains, consistent with its roles in adhesion and motility. Functionally, PZR serves as a multifunctional signaling hub, acting as both a receptor for concanavalin A (ConA) and a regulator of SH2 domain-containing protein tyrosine phosphatase-2 (SHP-2) and Src family kinases. ConA binding triggers c-Src activation, leading to PZR autophosphorylation and subsequent recruitment of SHP-2. Its intracellular immunoreceptor tyrosine-based inhibitory motifs (ITIMs) further mediate interactions with Src kinases and SHP-2, driving oncogenesis, immunomodulation, and antiviral responses. Post-translational modifications, including phosphorylation and glycosylation, enhance its protein-binding capacity, enabling broad influence over physiological and pathological processes, particularly in tumor microenvironment signaling and cellular fate regulation. Initially implicated in Noonan syndrome and schizophrenia, recent studies highlight PZR as a critical regulator of cancer cell adhesion and migration, with dysregulation accelerating disease progression. This review systematically analyzes the structural and functional properties of PZR, explores its disease-associated molecular mechanisms, and integrates emerging evidence to propose PZR as a promising therapeutic target. By delineating its signaling networks and pathophysiological roles, we provide a framework for advancing diagnostic and therapeutic strategies targeting PZR-related disorders. - Source: PubMed
Publication date: 2025/08/12
Wang Heng PingSha WanLiFu YingWang Huiyan - The tumor microenvironment promotes cancer progression in part by supporting cancer stem cells (CSC). In colorectal cancer (CRC), progastrin (PG), an orphan growth factor secreted by tumor cells within the tumor and its microenvironment, maintains CSCs by unidentified mechanisms. Here, the orphan receptor Protein Zero-Related protein (PZR) is identified as an essential component of PG activity and demonstrated its utility as a therapeutic target. PZR is essential for growth of PG-expressing tumors, while genetic inactivation in mice of Mpzl1, which encodes PZR, disrupted chemically-induced colon transformation. Mechanistically, PG binds cellular glycosylated and dimeric PZR and promotes SHP2/SRC/β-catenin-dependent CSC-like signaling. Blocking PZR by monoclonal antibodies inhibited PG-dependent expansion of tumoroids derived from murine intestinal tumors and patient-derived CRC cell lines, while in mice, it reduced adenoma formation triggered by Apc loss in stem cells and disrupted the tumor-initiating capacity of PG-expressing CRC cells. High GAST (which encodes PG) and MPZL1 transcript levels in primary colon cancer patients is predictive of worse prognosis. Collectively, these findings support the inhibition of PZR as a potential targeted treatment of PG-expressing CRC. - Source: PubMed
Publication date: 2025/08/03
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