Ask about this productRelated genes to: CD99L2 Blocking Peptide
- Gene:
- CD99L2 NIH gene
- Name:
- CD99 molecule like 2
- Previous symbol:
- MIC2L1
- Synonyms:
- CD99B
- Chromosome:
- Xq28
- Locus Type:
- gene with protein product
- Date approved:
- 2002-02-28
- Date modifiied:
- 2015-11-30
Related products to: CD99L2 Blocking Peptide
Related articles to: CD99L2 Blocking Peptide
- - Source: PubMed
Publication date: 2026/06/22
Kang MinjiYoon Sang HoKang MinkyungPark Seung PyoSong Woo SeokKim JunghoLee SeunghaPark Da-HaSong Jae-ManKim BeomsuePark Kyung HeeJoe Eun-HyeWoo Hyun GooKaang Bong-KiunHan DohyunLee Yong-SeokKim Myoung-HwanSuh Young Ho - The onset of blood circulation is a pivotal developmental event, yet the molecular mechanisms that enable erythrocytes to disengage from the endothelium and enter the bloodstream remain unclear. Here, we identify CD99L2 as a mechanoresponsive adhesion regulator, transiently induced in primitive erythrocytes by shear stress-activated Piezo1 signaling. Using zebrafish and mouse models, we show that CD99L2 is essential for erythrocyte de-adhesion and circulation entry. Loss of CD99L2 leads to aberrant nuclear translocation of β-catenin, activation of Rap1 signaling, and persistent expression of adhesion molecules, culminating in erythrocyte retention, impaired maturation, and hemolytic anemia. Mechanistically, CD99L2 binds and anchors β-catenin at the membrane, and shear-induced Piezo1 activation promotes its expression during a narrow developmental window. This pathway is conserved in mice and modulated by biomechanical forces, unveiling a mechanism that couples hemodynamic force to erythrocyte adhesion control during the initiation of blood flow. - Source: PubMed
Publication date: 2026/03/30
Lu JingaoZhao JunTang XinZhu EnteXu JinChen XiaohuiWang QiangHuang ZhibinMa NingZhang WenqingLiu Wei - Most patients with a rare movement disorder (MD) do not receive a molecular diagnosis, and the underlying genetic variants and mediating genes remain elusive. Here, we evaluate the diagnostic accuracy of conventional and next-generation sequencing-based genetic testing strategies in a cohort of 2,811 individuals with ataxia, spastic paraplegia and dystonia. Exome sequencing establishes genetic diagnoses in 19.3% of cases, and specificity of phenotypic features and age at testing are positive predictors. Genome analysis 'beyond the exome' increases the diagnostic yield by 7.5%, mostly due to the improved detection of structural variants and repeat expansions. Unsolved cases are included in the Solve-RD cohort and subjected to gene-burden analysis, providing evidence for loss-of-function variants in X-chromosomal CD99L2 causing spastic ataxia. Cellular studies show that the transmembrane protein CD99L2 occurs mainly in a ubiquitinated form and serves as an activating interactor of the calcium-dependent protease CAPN1. Ablation of cytoplasmic or extracellular domains of CD99L2 leads to its intracellular mislocalization and abrogation of its interplay with CAPN1. Transcriptome analysis in CD99L2 patient-derived fibroblasts reveals synaptic function-specific disturbances. Impaired CAPN1 activation and dysregulation of downstream neuronal pathways constitute the likely molecular cause for neurodegeneration. - Source: PubMed
Publication date: 2026/02/14
Menden BenitaIncebacak Eltemur Rana DDemidov GermanSturm MarcPark JoohyunHuridou ChrisovalantouFath FlorianNümann AstridBaumann AlexanderDiets Illja JDufke ClaudiaRegensburger MartinRönnefarth MariaWilke Veravan Os NienkeVielhaber StefanRattay Tim WKohl ZachariasPeralta SusanaPereira Sena PriscilaKellner MelanieWeissert NadineTraschütz AndreasZeltner LenaBoelmans KaiDeininger NatalieSchütz LeonGross CasparHinojosa Amaya Ana BeatrizRaupach KatrinHengel HolgerHarmuth FlorianAdmard JakobBader IngridBaumann SarahBender FriedemannBevot AndreaBischoff AlmutBoschann FelixBuchert RebeccaBuchzik DanielCasadei NicolasCatarino Claudia BCordts IsabellCremer KirstenDoebler-Neumann MarionEhmke NadjaElbracht MiriamFalb Ruth JFeindt ThomasFleszar ZofiaGerstner LeaGläser DieterGrasshoff UteGrosch SarahGrundmann KathrinGutschalk AlexanderHaaga ManjaHayer StefanieHehr UteHellenbroich YorckHenn WolframHerr BarbaraHerzog RebeccaHorber VeronkaDeppe JonasKaiser NadjaKehrer ChristianeKehrer MartinKern JanKeßler ChristophKhuller KatharinaKlinkhammer HannahKotzaeridou UraniaKrawitz PeterKreiss MartinaKüpper HannaKuster AliceLaugwitz LuciaLesemann AnneLichey NadineLinden TobiasMacek BorisMagg JanineMangold ElisabethManka EvaMarquardt IrisMehnert KarlMengel DavidMorlot SusanneOehl-Jaschkowitz BarbaraPauly Martje GPhilipp MelanieRadelfahr FlorentineRautenberg MarenRiess AngelikaSaft CarstenSchlotter-Weigel BeateSchmidt AxelSchwaibold Eva M CSpahlinger VeronikaSpranger StephanieSteiner Katharina MarieStendel ClaudiaThieme AndreasTzschach AndreasVelic AnaWiethoff SarahWilke CarloZüchner StephanZittel Simone Husain Ralf ADeschauer MarcusDistelmaier FelixDufke AndreasGraessner HolmHemmer BernhardJacobi HeikeKlockgether ThomasKlopstock ThomasKobeleva XeniaKorenke Georg-ChristophKuechler AlmaKuhlenbäumer GregorKurth IngoNguyen Huu PhucWunderlich GilbertZeuner Kirsten EKlebe StephanAuer-Grumbach MichaelaButryn MichaelaWinkler JürgenTimmann DagmarSynofzik Matthisvan de Warrenburg BartSchüle RebeccaSchöls LudgerOssowski StephanRiess OlafWeber Jonasz JHaack Tobias B - Pancreatic adenocarcinoma (PAAD) is characterized by complex molecular alterations in cell adhesion molecules (CAMs) that influence tumor progression and treatment resistance. Identifying clinically relevant CAM signatures could improve patient stratification and therapeutic strategies. In this study, we integrated bulk RNA-seq data from TCGA and ICGC with single-cell RNA-seq data to identify survival-associated CAM genes and define molecular subtypes using consensus clustering. We identified 22 CAM genes associated with prognosis and established three molecular subgroups with distinct clinical and immune characteristics. An 11-gene CAM-based risk model (CDH3, CLDN16, CLDN3, CLDN15, ITGB1, NCAM1, SDC1, CD99L2, SLITRK2, LRRC4B, CD58) demonstrated strong prognostic performance across cohorts and effectively predicted chemotherapy and immunotherapy responses. High-risk patients exhibited extracellular matrix activation, immune evasion, and poor response to PD-1/PD-L1 blockade. Single-cell analysis revealed distinct expression patterns of CAM genes across malignant and epithelial compartments. Functional validation confirmed CLDN16 as a pro-tumorigenic factor enhancing invasiveness and reducing apoptosis. These findings highlight the potential of CAM-based signatures to classify PAAD subtypes, predict prognosis, and inform personalized therapeutic strategies. - Source: PubMed
Publication date: 2025/12/18
Zhuo ZeweiLuo JianmingLiang GuanpengLi JiahaoYang QiHuang Lin - Glioblastoma Multiforme (GBM) is a highly aggressive and fatal brain malignancy, with Temozolomide (TMZ) serving as the first-line chemotherapeutic treatment. However, over 50% of patients do not respond to TMZ, and the underlying mechanisms remain unclear. This study utilized the GeCKO library to identify novel genes involved in TMZ resistance and to explore their functions. - Source: PubMed
Sun ZeenCui MengkeDeng ZenghaoZhou LuZeng FeiyueLiu ZhaoqianLiu Yingzi