Ask about this productRelated genes to: LAPTM4B antibody
- Gene:
- LAPTM4B NIH gene
- Name:
- lysosomal protein transmembrane 4 beta
- Previous symbol:
- -
- Synonyms:
- LC27
- Chromosome:
- 8q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 2002-12-16
- Date modifiied:
- 2008-08-11
Related products to: LAPTM4B antibody
Related articles to: LAPTM4B antibody
- Lysosomal-associated protein transmembrane (LAPTM) family members-including LAPTM4A, LAPTM4B, and LAPTM5-are key regulators of lysosomal integrity, autophagy-lysosome flux, lipid metabolism, and immune responses. Dysregulation of LAPTM proteins contributes to neurological disorders such as Alzheimer's disease, Parkinson's disease, ischemic stroke, and gliomas, affecting neuronal survival, glial homeostasis, neuroinflammation, and tumor progression. In this review, we summarize recent insights into the structural features and molecular mechanisms of LAPTM proteins in the nervous system and highlight their therapeutic potential in promoting protein aggregate clearance, mitigating oxidative stress, regulating microglial polarization, and enhancing tumor immunotherapy. Future research integrating gene therapy, small-molecule modulators, multi-omics profiling, and advanced delivery platforms may enable translation of LAPTM-targeted interventions into clinical practice, offering new avenues for diagnosis, prognosis, and treatment of neurological diseases. - Source: PubMed
Wang ZitongPan YangShu MinZou Li - Relapse remains the leading cause of mortality in acute myeloid leukemia (AML), largely due to the persistence of therapy-resistant leukemia stem cells (LSCs). However, surface determinants that sustain LSC function and disease aggressiveness remain incompletely defined. Here, we identify the tetraspanin CD81 as a regulator of LSC function, progression and treatment resistance in AML. Analysis of retrospective patient cohorts revealed that high CD81 surface expression is associated with relapse and adverse clinical outcomes in non-core-binding factor AML. Functional studies demonstrated that elevated CD81 expression promotes chemoresistance and enhances leukemic engraftment in immunodeficient mouse models. In vivo gain- and loss-of-function approaches further established that CD81 drives increased leukemia burden and aggressive disease behavior. Notably, CD81 was enriched within LSC-containing subpopulations, where its expression supported LSC maintenance and resistance to chemotherapy. Mechanistically, CD81 promotes chemoresistance and leukemic aggressiveness through pathways linked to LAPTM4B-mediated STAT3 signaling and enhanced adhesion-dependent cellular interactions. These effects were accompanied by increased migration, invasion, and formation of filopodia-like membrane protrusions. Importantly, therapeutic immunotargeting of CD81 significantly reduced leukemic burden while exhibiting a manageable toxicity profile in preclinical models. Collectively, these findings establish CD81 as a clinically relevant surface marker associated with AML relapse and identify CD81-dependent signaling as a therapeutic vulnerability for targeting LSCs and preventing disease recurrence. - Source: PubMed
Publication date: 2026/04/21
Gonzales FannyPeyrouze PaulineLaurent DjohanaBoyer ThomasBoukrout NihadCouturier CyrilHoudiard SoizicLisi VéroniqueBarthélémy AdelineSevrin FrançoisPlesa AdrianaBongiovanni AntoninoPottier NicolasPreudhomme ClaudeLavallée Vincent-PhilippeGeles KonstantinosDuployez NicolasBerthon CélineRoumier ChristopheCheok Meyling - This study aims to reveal the potential mechanism and potential prognostic markers of programmed cell death (PCD) genes associated with 6-acetoxy-anopterine (6-AA) resistance in prostate adenocarcinoma (PRAD). - Source: PubMed
Publication date: 2026/01/31
Cheng JieMao Dongdong - Lysosomal-associated protein transmembrane (LAPTM) family members-LAPTM4A, LAPTM4B, and LAPTM5-regulate lysosomal integrity, autophagy-lysosome flux, lipid homeostasis, and immune signaling, pathways increasingly implicated in neurological disease. This review synthesizes structure-function evidence for LAPTM proteins and examines how their dysregulation contributes to Alzheimer's and Parkinson's disease, ischemia-reperfusion injury, and gliomas. Based on a targeted narrative analysis of primary and translational studies, we highlight that LAPTM proteins influence lysosomal acidification and membrane stability, endolysosomal trafficking, and ceramide/ion handling, thereby shaping protein aggregate clearance, oxidative stress responses, and microglia/macrophage polarization. Preclinical data link LAPTM5 to stroke outcomes via stress-kinase and lysosomal pathways, while LAPTM4A and LAPTM4B associate with glioma progression, immune evasion, and therapy resistance. Overall, LAPTM proteins represent promising biomarkers and therapeutic targets, warranting cell-type-resolved validation and central nervous system (CNS)-optimized delivery strategies, including gene therapy, small-molecule/degrader approaches, and multi-omics-guided patient stratification. - Source: PubMed
Publication date: 2026/02/10
Wu BowenNiu ZhenyanSui Yanfang - Acute myeloid leukemia (AML) remains a high-risk hematologic malignancy due to frequent relapse and therapeutic resistance. Although induction therapy can achieve cytological remission, a fraction of leukemic cells (minimal residual disease, MRD) persists within the protective bone marrow (BM) microenvironment. MRD is heterogeneous and may include subclones with intrinsic survival features present before therapy. Among these, rare BM-resident leukemic cells (BMresLC) may represent pre-adapted precursors of MRD, maintained in a low-proliferative (Ki67) or quiescent state. We previously showed that calcium signaling through ORAI1-dependent store-operated calcium entry (SOCE) contributes not only to AML stemness and drug resistance but also to the regulation of the G0-G1 cell-cycle transition and the emergence of slow-cycling leukemic cells. With this study, we have characterized the stemness and calcium signature of BMresLC before any therapeutic intervention. Our results, beyond further characterizing a population of cells rarely studied, could thus pave the way to new therapeutic opportunities combining current treatments with the targeting of relevant pathways highlighted by our work. - Source: PubMed
Publication date: 2026/01/09
Titah SofiaGuillemette AurélieLewuillon ClaraShaik Faruk AzamBerthon CélineGoursaud LaureTardivel MeryemBongiovanni AntoninoChauvet PaulJouy NathaliePeyrouze PaulineCheok MeylingBrinster CarineManier SalomonTarhan Mehmet ÇagatayLemonnier LoïcQuesnel BrunoTouil Yasmine