Ask about this productRelated genes to: NOMO1 antibody
- Gene:
- NOMO1 NIH gene
- Name:
- NODAL modulator 1
- Previous symbol:
- -
- Synonyms:
- PM5
- Chromosome:
- 16p13.11
- Locus Type:
- gene with protein product
- Date approved:
- 2004-09-10
- Date modifiied:
- 2014-11-19
Related products to: NOMO1 antibody
Related articles to: NOMO1 antibody
- Combination therapies are widely used in acute myeloid leukemia (AML), but systematic datasets capturing proteome-wide responses to multi-drug perturbations remain limited. Here we present CoPISA (Combinatorial Proteome Integral Solubility/Stability Alteration), a quantitative proteomics assay designed to profile protein solubility and stability responses to single and combined drug treatments. The dataset includes two AML drug pairs (LY3009120-sapanisertib and ruxolitinib-ulixertinib) applied to four AML cell lines (MOLM-13, MOLM-16, SKM-1, and NOMO-1) under control, single-agent, and combination conditions in both lysate and intact-cell formats. Thermal solubility profiling coupled with TMT-based multiplexed LC-MS/MS generated 16 TMT16-plex experiments comprising 192 LC-MS/MS raw files, providing deep proteome coverage across treatments and biological contexts. The resource includes raw and processed proteomics data, detailed experimental metadata in Sample and Data Relationship Format (SDRF), and reproducible analysis scripts for reporter normalization, protein-level aggregation, statistical modeling, and classification of combinatorial response patterns. The experimental design enables identification of proteins responding uniquely to combination treatments as well as overlapping single-agent effects. Technical validation demonstrates reproducible quantification across multiplex experiments and assay formats. All data are publicly available through the PRIDE repository (PXD066812) together with analysis code, enabling independent reanalysis and method development. This dataset provides a benchmark resource for studying proteome responses to drug combinations, comparing lysate and intact-cell perturbation profiles, developing computational approaches for combinatorial target inference, and supporting training in computational proteomics. - Source: PubMed
Publication date: 2026/06/29
Zangene EhsanGholizadeh ElhamVadadokhau UladzislauRitz DaniloSaei Amir AJafari Mohieddin - Mesothelin (MSLN) is a glycosylphosphatidylinositol-anchored cell surface protein that is overexpressed in several solid tumors and in one-third of pediatric acute myeloid leukemia (AML) cases. It represents a validated immunotherapeutic target owing to its lack of expression in normal bone marrow. The function of MSLN in AML is unknown, but it is implicated to regulate adhesion in solid tumors through interaction with its only known binding partner, MUC16/CA125. This study uses CRISPR/Cas9 mutagenesis to generate knockout (KO) of MSLN in NOMO-1 and a MSLN-expressing patient-derived xenograft model to investigate its biological role in AML. We show that MSLN-KO cells proliferate slower, have reduced mitochondrial metabolism, are arrested in G1 cell cycle phase, adhere less to extracellular matrix in vitro and engraft slower in vivo. MSLN-KO cells also exhibit increased sensitivity to Ara-C and reduced extracellular matrix-mediated chemoprotection. Using an unbiased approach, we identify Src-family kinase member LYN, and guanine nucleotide-binding protein G(i) alpha subunit proteins, GNAI1, GNAI2, and GNAI3 as novel binding partners of MSLN in AML and show that pharmacological or genetic inhibition of LYN signaling restores NOMO-1 cell sensitivity to Ara-C. Together, these findings demonstrate that MSLN functions as an oncogenic driver in AML and reveal a previously unrecognized MSLN-LYN signaling axis, the therapeutic targeting of which may enhance responses to chemotherapy. - Source: PubMed
Publication date: 2026/03/20
Faust Joshua RHamill DarcyKolb E AndersStevens Alexandra MGopalakrishnapillai AnilkumarBarwe Sonali P - Prostate-Specific Antigen (PSA) is widely used for Prostate Cancer (PCa) screening, but its low specificity often leads to false-positive results and unnecessary biopsies. To address this issue, we introduced Age-Adjusted Prostate-Specific Antigen Density (A-PSAD) as a potential biomarker to improve screening accuracy for PCa and Clinically Significant Prostate Cancer (csPCa). - Source: PubMed
Publication date: 2026/01/28
Liu ZiyangShan JiahaoZhang QiangGao YuLv ZhiyongMa LianghongShi Hongbin - Acute myeloid leukemia (AML) is a hematological malignancy with poor treatment outcomes and high mortality rates. AML progression is influenced by signalling events facilitated by small GTPases anchored to cellular membranes via post-translational modification with geranylgeranyl pyrophosphate (GGPP). The disruption of GGPP biosynthesis, and the resulting intracellular reduction of key geranylgeranylated GTPases, represents an as yet unleveraged strategy for the treatment of cancer. Here we show compound CML-07-119, a selective inhibitor of GGPP synthase (GGPPS), to display an EC potency in the nanomolar range and to induce targeted cell death in several AML cell lines, including those harbouring TP53 mutations. Antitumor efficacy was also observed with CML-07-119 in a mouse xenograft model engrafted with AML NOMO-1 cells, equivalent to the drug cytarabine. Bone-marrow and splenocyte cells harvested from mice treated with CML-07-119 displayed significantly higher concentration of unprenylated RAP1A as compared to the controls, demonstrating the expected biochemical outcome of in vivo GGPPS inhibition. X-ray crystallography and cryo-EM were used to determine high resolution structures of the unliganded GGPPS and the GGPPS/CML-07-119 complex. These structures revealed that the inhibitor occupies a previously proposed product inhibitory channel of the enzyme, and modulates previously unknown conformational states of GGPPS quaternary structure. This work validates GGPPS inhibition as potential novel mechanism for the treatment of AML. - Source: PubMed
Publication date: 2025/12/17
Tsantrizos YoulaFerens FraserWaller DanielBoutin RebeccaLee Hiu-FungSaba-El-Leil MarcTremblay MathieuGuan Tian LaiSkorey KathrynSebag MichaelWiita ArunLemieux M Joanne - There remains an unmet clinical need for improved treatment strategies in Acute Myeloid Leukemia (AML). Although radiopharmaceutical therapies targeting non-cancer-selective antigens have shown promise in AML, their clinical utility is often limited by prolonged bone marrow suppression. Using a unique proteomics-based strategy, we recently identified the active conformation of integrin-β2 (aITGB2) as a novel, tumor-selective target for AML. Importantly, this conformational epitope is expressed widely on AML cells but minimally on normal marrow progenitors/healthy tissues. Here we first confirmed widespread aITGB2 expression on AML tumors that was largely independent of tumor genotype or prior therapeutic regimen. We developed diagnostic and therapeutic radiopharmaceuticals targeting aITGB2 utilizing a conformation-specific antibody (clone 7065). PET/CT imaging with Zr and Ce-labeled 7065 in AML models revealed high target-mediated uptake, greater than that compared to standard of care [F]-FDG. PET/CT imaging with [Zr]DFO*-7065 showed reduced binding to normal bone marrow and immune cells in humanized immune system mice compared to [Zr]DFO*-anti-CD33. For therapy, we developed [Ac]Macropa-PEG-7065 using an optimized chelator-linker combination. Treatment with [Ac]Macropa-PEG-7065 in Nomo-1 and PDX AML disseminated models delayed tumor growth and improved overall survival compared to controls, including [Ac]DOTA-anti-CD33, a clinical stage-radioimmunotherapy under evaluation in AML. Relapsed tumors demonstrated persistent aITGB2 expression, supporting continued development of fractionated dosing schemes, and proteomics analysis indicated activation of TCA cycle and carbon metabolism pathways, consistent with therapy-induced stress responses. These findings highlight [Zr]DFO*-7065 and [Ac]Macropa-7065 as a promising aITGB2-targeted theranostic pair with potential for imaging and treatment in future clinical translation. - Source: PubMed
Publication date: 2025/10/29
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