CDCP1 protein
- Known as:
- CDCP1 protein
- Catalog number:
- 80R-4403
- Product Quantity:
- 10 ug
- Category:
- -
- Supplier:
- Fitzgerald
- Gene target:
- CDCP1 protein
Related genes to: CDCP1 protein
- Gene:
- CDCP1 NIH gene
- Name:
- CUB domain containing protein 1
- Previous symbol:
- -
- Synonyms:
- CD318, SIMA135
- Chromosome:
- 3p21.31
- Locus Type:
- gene with protein product
- Date approved:
- 2005-02-24
- Date modifiied:
- 2016-10-05
Related products to: CDCP1 protein
Related articles to: CDCP1 protein
- Multiple sclerosis (MS) disease activity and treatment response may be influenced by systemic health factors, including cardiometabolic disease (CMD). This study evaluated how CMD influences inflammatory protein profiles and whether CMD modifies the effect of disease-modifying therapy (DMT). A retrospective study was conducted within a single academic MS center. All participants underwent commercial multi-analyte proteomic testing (Octave® Bioscience). CMD was defined as hypertension, type 2 diabetes mellitus, and/or dyslipidemia. Four groups were analyzed: untreated without CMD, untreated with CMD, DMT-treated without CMD, and DMT-treated with CMD. A multivariable variability index (MVI) was calculated across 18 age- and sex-adjusted proteins, and CMD burden (one, two, or three conditions) was assessed. A total of 287 MS individuals were included (84% White, 78% female). Among untreated individuals, those with CMD demonstrated significantly higher concentrations of proteins associated with acute MS disease activity, including MIP 3-alpha (CCL20) (p = 0.0078), CUB domain-containing protein 1 (CDCP1) (p = 0.0176), and TRAIL-R1 (TNFRSF10A) (p = 0.0002). In treated individuals, CMD was associated with higher levels of monokine induced by gamma interferon (CXCL9) (p = 0.0025), NfL (p = 0.0201), serpin family A member 9 (p = 0.0291), and TRAIL-R1 (p = 0.0002), as well as lower levels of protogenin (p = 0.0376). MVI values were elevated in both CMD groups. CMD was associated with higher odds of prior relapse and/or MRI activity within two years before proteomic testing (OR 5.48, 95% CI: [1.18-25.40], p = 0.0227). Protein concentrations increased with greater CMD burden. Clinically measurable proteins associated with acute MS disease activity are elevated in individuals with CMD and increase with comorbidity burden, in both DMT-treated and untreated groups. - Source: PubMed
Publication date: 2026/09/10
Okuda Darin TBurgess Katy WWright Crystal MJones-McCreary Morgan CHuddleston Isabella JSantoyo Jose RPunnen Tom GSguigna Peter VTardo Lauren MLebrun-Frénay ChristineStüve OlafTran Diem HMoog Tatum M - Acute inflammatory relapses in primary CNS demyelinating diseases, including relapsing multiple sclerosis (RMS), MOG-antibody-associated disease (MOGAD), and neuromyelitis optica spectrum disorder (NMOSD), drive hospitalization, disability, and socioeconomic burden. Blood-based biomarkers are increasingly used for relapse detection and treatment monitoring. - Source: PubMed
Publication date: 2026/09/07
Chumakova Anastasia PDemetriou MichaelSy Michael - The spatial organization of membrane proteins is an underexplored dimension of cell surface biology. Spatial proximity shapes cellular function and therapeutic targetability, yet efforts to identify tumour-associated antigens (TAAs) have largely focused on expression alone. Here, we developed an industrialized surface protein proximity-mapping workflow to interrogate TAAs within their membrane microenvironments. Using this workflow, we generated 248 proximity maps across 12 receptor tyrosine kinases and 28 tumour cell systems. The resulting atlas enabled the development of MetaMap, a correlation-based analytical framework that defines spatial protein communities and infers conserved proximity relationships among non-targeted proteins, and establishes the concept of tumour-associated proximity antigens (TAPAs), a class of co-targets defined by disease-specific spatial proximity to TAAs rather than expression alone. Integrating these proximity-derived relationships within a multimodal prioritization framework, we identified and validated EGFR-CDCP1 as a TAA-TAPA pair that enhances tumour cell killing across therapeutic modalities. Together, this work advances disease-associated membrane proximity as a guiding principle for the design of precision multispecific therapeutics. - Source: PubMed
Publication date: 2026/09/09
Scandore CodyMalone Clare FMay Christopher Kde Regt Anna KGuernsey JeffMa HayleyDephoure NoahSetter BenHowell Rebecca AJohnson Kendall RFarr Carol LRomero SophiaVignale LydiaVittum TaliDawson EmmaHabtetsion TsadikNardi FrancescaWoodruff BrianMathay MartinSwanson JuliaRusnak MikaelaTon QuynhFarahani Payam EGene Robert WMisurelli JasonCaldwell ZachXu HengyuHornsby MichaelGavin Marc AKlock Heath EEryilmaz ErtanHolland Pamela MLesley Scott AOslund Rob CFadeyi Olugbeminiyi O - Triple-negative breast cancer (TNBC) is associated with recurrence, metastasis, and limited durable responses to immunotherapy, in part due to persistence of breast cancer stem cells (BCSCs). We investigated whether CD6-directed immunotherapy with the monoclonal antibody UMCD6 enhances immune-mediated killing and alters function of BCSC in stem cell-enriched TNBC models. The SUM-149 and SUM-159 cell lines were analyzed for CD6 ligand expression, cocultured with human peripheral blood mononuclear cells (PBMCs) treated with UMCD6, pembrolizumab, or isotype control, and assessed by live-cell cytotoxicity imaging, flow cytometry, soft agar colony formation, and extreme limiting dilution sphere assays. Both TNBC lines co-expressed the CD6 ligands CD44, CD166/ALCAM, and CD318/CDCP1. UMCD6 significantly increased PBMC-mediated apoptosis and reduced tumor cell survival in both models, with greater activity than pembrolizumab under these in vitro conditions. In surviving SUM-159 cells, UMCD6 reduced the ALDH population wit×hout significantly altering CD44CD24 frequency, indicating preferential effects on a distinct stem-like compartment. Functionally, UMCD6 decreased anchorage-independent colony formation and reduced sphere-forming frequency from 1/33.6 to 1/68.3 cells ( = 0.0186). These findings identify the CD6 ligand axis as a therapeutic vulnerability in BCSC-enriched TNBC and support further preclinical evaluation of CD6-directed immunotherapy as a strategy to enhance antitumor immunity while limiting tumor-initiating capacity. - Source: PubMed
Publication date: 2026/08/17
Gurrea-Rubio MikelSloan SophieChada AdityaAmarista Camila IMaeda KoheiCampbell Phillip LTsou Pei-SuenCooney Laura AWicha Max SFox David A - The CD6 cell surface glycoprotein is expressed by almost all T cells, a small subset of B cells and a substantial proportion of human natural killer (NK) cells. CD6 has multiple ligands and multiple functional epitopes. It is a component of the immunological synapse, and can positively or negatively influence signal transduction in T cells through complex interactions with multiple kinases and adapter molecules. Antibodies to CD6 are effective in the treatment of autoimmune diseases in experimental systems and in humans. The recent discovery that CD318 (CDCP1), a driver molecule in many cancers, is a ligand for CD6 has prompted investigation of CD6 as a possible new target for immunotherapy of cancer. A monoclonal antibody to CD6 rapidly internalizes CD6 and alters gene expression in CD8+ T cells and NK cells to augment the cytotoxicity of human lymphocytes to human cancer cells from a range of neoplasms. This review, using a question and answer format, describes recent work on anti-CD6 as a candidate immunotherapy for cancer as well as relevant advances in our understanding of other aspects of the biology of CD6, and explores the possibility that this approach could avoid the autoimmune complications that are encountered with checkpoint inhibitor treatment of cancer. - Source: PubMed
Publication date: 2026/08/11
Fox David AGurrea-Rubio Mikel