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
- 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
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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 - Cd99 molecule-like 2 (Cd99l2) is a type I transmembrane protein that plays a role in the transmigration of leukocytes across vascular endothelial cells. Despite its high expression in the brain, the role of Cd99l2 remains elusive. We find that Cd99l2 is expressed primarily in neurons and positively regulates neurite outgrowth and the development of excitatory synapses. We demonstrate that Cd99l2 inversely regulates the expression of immediate-early genes (IEGs), including Arc, Egr1, and c-Fos, by inhibiting the activity of the transcription factors CREB and SRF. Neuronal inactivation increases the transport of Cd99l2 to the cell surface from recycling endosomes, thereby enhancing Cd99l2-mediated inhibitory signaling. Additionally, Cd99l2 knockout mice exhibit impaired excitatory synaptic transmission and plasticity in the hippocampus, along with deficits in spatial memory and contextual fear conditioning. Based on these findings, we propose that neuronal Cd99l2 functions as a synaptic cell adhesion molecule that inversely controls neuronal activation. - Source: PubMed
Publication date: 2025/01/13
Kang MinjiYoon Sang HoKang MinkyungPark Seung PyoSong Woo SeokKim JunghoLee SeunghaPark Da-HaSong Jae-ManKim BeomsuePark Kyung HeeJoe Eun-HyeWoo Hyun GooPark Seong HoeKaang Bong-KiunHan DohyunLee Yong-SeokKim Myoung-HwanSuh Young Ho