Ask about this productRelated genes to: CDR2L antibody
- Gene:
- CDR2L NIH gene
- Name:
- cerebellar degeneration related protein 2 like
- Previous symbol:
- -
- Synonyms:
- HUMPPA
- Chromosome:
- 17q25.1
- Locus Type:
- gene with protein product
- Date approved:
- 2005-11-14
- Date modifiied:
- 2016-03-31
Related products to: CDR2L antibody
Related articles to: CDR2L antibody
- Immunogenicity prediction is widely used in the developability assessment of antibodies, and many marketed and clinical-stage therapeutics have a predicted T-cell epitope in the second complementary-determining region of their light chain (CDR2L). To investigate such CDR2Ls in more detail, we identified an antibody with a CDR2L for which a patient had developed treatment-emergent (TE) anti-drug antibodies (ADAs) in a clinical setting. With this, we establish the importance of predicted T-cell epitopes in CDR2L. In the course of deleting the T-cell epitope, we decided to aim for a solution that can be applied broadly to facilitate larger high-throughput discovery campaigns. For this purpose, we have developed a double-mutation scheme that targets AHo67 (Kabat51) and AHo68 (Kabat52) in the CDR2L. This 67G-68G mutation scheme was applied to all light chain sequences of a tri-specific single-chain diabody fused to a single-chain variable fragment (scMATCH3™) antibody for which TE ADAs had been observed. Analyses of patient sera showed that introduction of 67 G-68 G in CDR2L in combination with our previously described T101S-T146K (Kabat: T87S-T110K) framework mutations led to a scMATCH3 antibody with significantly reduced levels of both preexisting and TE ADA reactivities. For a diverse collection of single-chain variable fragments, application of the 67 G-68 G mutation scheme was experimentally seen to not substantially affect the functional or biophysical properties of the molecules, suggesting that this mutation scheme may be applicable to the improvement of therapeutic safety of antibodies of many types, with CDR2L-associated immunogenicity. - Source: PubMed
Publication date: 2025/12/22
Johansson Maria UKerschenmeyer AnneCarella AlessandraCarnal SimonSchmidt Yannikde Felice AlessandraMahler DanaThomas MarcSpiga Fabio MarioTietz JuliaWeinert ChristopherHess ChristianUrech DavidWarmuth Stefan - Anti-Yo antibodies, which target the onconeural antigen cerebellar degeneration-related 2-like (CDR2L), have been only sporadically reported in patients with post-immune checkpoint inhibitor (post-ICI) neurological syndromes. - Source: PubMed
Publication date: 2025/10/26
Farina AntonioPeter EliseBillet NolwennVillagrán-García MacarenaRogemond VéroniqueNicola CelesteTreilleux IsabelleDo Le-DuyBenaiteau MariePicard GéraldineMeyronet DavidPissaloux DanielVillard MarineWucher ValentinHonnorat JérômeJoubert BastienDesestret Virginie - The increasing prevalence of gestational diabetes mellitus (GDM), particularly among overweight or obese individuals, poses significant health risks. Excess iron contributes to oxidative stress, inflammation, and disruptions in immune and metabolic functions in GDM. Deferoxamine (DFO), an iron chelator, may offer a therapeutic solution by restoring immune and metabolic balance. - Source: PubMed
Publication date: 2025/09/29
Zhang MinWei NaLin RongXu YueZhang QingfuJia LinaZhang XiaotongYang Xiaojing - The ER relies on the microtubule cytoskeleton for the organization of its extended membrane network, but how microtubule-based motors contribute remains unclear. Using biochemical and cell-based assays, we identify cerebellar degeneration-related protein 2 (CDR2) and its paralog CDR2-like (CDR2L), onconeural antigens with poorly understood functions, as ER adaptors for cytoplasmic dynein-1 (dynein). We demonstrate in human cancer cells that CDR2 is recruited by the integral ER membrane protein kinectin (KTN1) and that double knockout of CDR2 and CDR2L enhances KTN1-dependent ER sheet stacking, reversal of which by exogenous CDR2 requires its dynein-binding CC1 box motif. Exogenous CDR2 expression additionally promotes CC1 box-dependent clustering of ER sheets near centrosomes. CDR2 competes with the eEF1Bβ subunit of translation elongation factor 1 for binding to KTN1, and eEF1Bβ knockdown increases endogenous CDR2 levels on ER sheets, inducing their centrosome-proximal clustering. Our study describes a novel molecular pathway that implicates dynein in ER sheet organization and may be involved in the pathogenesis of paraneoplastic cerebellar degeneration. - Source: PubMed
Publication date: 2025/07/10
Teixeira VanessaSingh KashishGama José BMoreira MatildeCelestino RicardoXavier Carvalho AnaPereira Paulo SAbreu Carla M CDantas Tiago JCarter Andrew PGassmann Reto - Emerging evidence suggests a bidirectional relationship between colorectal cancer (CRC) and type 2 diabetes mellitus (T2DM), yet the shared molecular mechanisms and prognostic biomarkers remain poorly characterized. This study aimed to identify novel biomarkers linking CRC and T2DM pathogenesis and evaluate their clinical utility in predicting therapeutic responses and survival outcomes. By integrating multi-omics data from public repositories and applying machine learning-driven feature selection, we identified three core biomarkers-FABP4,CDR2L,and FSTL3 that independently predicted overall survival in CRC patients with diabetes. A prognostic nomogram combining these biomarkers with clinicopathological variables (tumor stage, grade, and age) achieved high accuracy for 1-, 3-, and 5-year survival prediction. Functional characterization revealed strong associations between biomarker overexpression and tumor microenvironment remodeling, particularly through fibroblast-mediated immune cell recruitment and cross-talk with lymphocytes. Critically, low expression of these genes correlated with improved anti-PD-1 immunotherapy responses in an independent clinical cohort. Our findings establish FABP4, CDR2L, and FSTL3 as pivotal regulators at the CRC-diabetes interface, with dual utility as prognostic indicators and predictors of immunotherapy efficacy. - Source: PubMed
Publication date: 2025/07/01
Wu ZhaohuiCao LiuliuZhao Jie