CD222
- Known as:
- CD222
- Catalog number:
- 11-315-C100
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- Exbio
- Gene target:
- CD222
Related genes to: CD222
- Gene:
- IGF2R NIH gene
- Name:
- insulin like growth factor 2 receptor
- Previous symbol:
- -
- Synonyms:
- CD222, MPRI, MPR1, CIMPR, M6P-R, CI-M6PR, CI-MPR, MPR300
- Chromosome:
- 6q25.3
- Locus Type:
- gene with protein product
- Date approved:
- 1988-07-07
- Date modifiied:
- 2019-04-23
Related products to: CD222
Antibodies: Mouse Monoclonal to CD222 _ IGF2 receptor _ CIMPR, Species Reactivity: Human, Non-Human Primates, Clone: MEM-238, Isotype: IgG1Antibodies: Mouse Monoclonal to CD222 _ IGF2 receptor _ CIMPR, Species Reactivity: Human, Non-Human Primates, Clone: MEM-238, Isotype: IgG1Antibodies: Mouse Monoclonal to CD222 _ IGF2 receptor _ CIMPR, Species Reactivity: Human, Non-Human Primates, Clone: MEM-238, Isotype: IgG1Antibodies: Mouse Monoclonal to CD222 _ IGF2 receptor _ CIMPR, Species Reactivity: Human, Non-Human Primates, Clone: MEM-238, Isotype: IgG1Antibodies: Mouse Monoclonal to CD222 _ IGF2 receptor _ CIMPR, Species Reactivity: Human, Non-Human Primates, Clone: MEM-238, Isotype: IgG1Antibodies: Mouse Monoclonal to CD222 _ IGF2 receptor _ CIMPR, Species Reactivity: Human, Non-Human Primates, Clone: MEM-238, Isotype: IgG1Antibodies: Mouse Monoclonal to CD222 _ IGF2 receptor _ CIMPR, Species Reactivity: Human, Non-Human Primates, Clone: MEM-238, Isotype: IgG1Antibodies: Mouse Monoclonal to CD222 _ IGF2 receptor _ CIMPR, Species Reactivity: Human, Non-Human Primates, Clone: MEM-238, Isotype: IgG1Antibodies: Mouse Monoclonal to CD222 _ IGF2 receptor _ CIMPR, Species Reactivity: Human, Non-Human Primates, Clone: MEM-238, Isotype: IgG1Antibodies: Mouse Monoclonal to CD222 _ IGF2 receptor _ CIMPR, Species Reactivity: Human, Non-Human Primates, Clone: MEM-238, Isotype: IgG1CD222 IGF2R antibody Ab host: RabbitCD222 IGF2R antibody Ab host: RabbitCD222 IGF2R antibody Ab host: RabbitCD222 IGF2R antibody Ab host: RabbitCD222 IGF2R antibody Ab host: Rabbit Related articles to: CD222
- Pediatric-onset multiple sclerosis (PedMS) provides a unique opportunity to investigate MS pathogenesis because of the short interval between environmental exposures and disease onset. This study aimed to identify differentially methylated regions (DMRs) that mediate the interplay between environmental triggers and genomic factors in the early stages of the disease. - Source: PubMed
Publication date: 2026/09/25
Corona AndreaTosi MartinaZollo AlenBarizzone NadiaPomella NicolaSimone MartaProtti AlessandraBerardinelli Angela LuciaGallo AntonioCanavese CarlottaVecchio DomiziaCocco EleonoraMoiola LuciaConti Marta ZaffiraMalucchi SimonaPapa AmandaMingione AlessandraMonzani CorinneAnnovazzi PietroGrimaldi Luigi M ELanzillo RobertaRasia SarahBova Stefania MariaRavanini PaoloCaushi FjorildaTorri Clerici Valentina Liliana Adriana MariaSotgiu StefanoPriori AlbertoTrojano MariaAmato Maria PiaBergamaschi RobertoPilotto SilvyPozzilli CarloCottone SalvatoreSantangelo GiuseppeDe Luca GiovannaPugliatti MauraGhezzi AngeloD'Alfonso SandraMartinelli Boneschi Filippo - Overexpression and abnormal activation of membrane proteins promote malignant tumor cell proliferation, while traditional interventions are often limited by drug resistance caused by target mutations. Here, we designed a stimulus-responsive DNA tetrahedron lysosome-targeted chimera (tFNA-LYTAC) strategy for degrading embrane proteins. Two tetrahedra are modified with trivalent HER2 aptamers (tFNA1-Apt) and trivalent IGF2R aptamers (tFNA2-Apt), enabling targeted binding to HER2 and IGF2R, and are then self-assembled into tFNA-LYTAC under VEGF stimulation to promote HER2 degradation. The trivalent aptamer modification strategy significantly enhances the overall binding capacity of tFNA1-Apt to cells. Importantly, tFNA-LYTAC formed only in the presence of VEGF, integrating tetrahedral multivalent aptamer targeting with stimulus responsiveness to improve the degradation specificity. VEGF-responsive tFNA-LYTAC promoted HER2 degradation and suppressed the phosphorylation of key downstream signaling proteins. The study innovatively proposes a "target recognition-stimulus response-endocytic degradation" mode that selectively regulates membrane proteins through programmable multivalent aptamer nanostructures. - Source: PubMed
Song LuluZhou MiaomiaoWang YaGuo XiaoliYang XinyiHu YiqiongWang YifuYu SongchengLiu WeiHe Leiliang - In vitro embryo production (IVP) is a reproductive technology commonly used in the dairy cattle industry for various purposes, such as maximizing the genetic contributions of elite breeding animals. However, IVP has been often associated with increased frequency of Large Offspring Syndrome (LOS) cases, resulting in high calf mortality, welfare concerns, and economic losses. LOS is a developmental disorder in calves characterized by abnormally large birth weight and body size, often accompanied by organ enlargement and other abnormalities. Among the imprinted genes frequently dysregulated in LOS, IGF2R (insulin-like growth factor 2 receptor) is one of the most consistently affected genes. Therefore, the main objectives of this study were to perform a comprehensive characterization of LOS in calves, including an assessment of differences in organ development, physiological parameters, and histopathological examinations between healthy and LOS-affected calves, and evaluate factors influencing its expression in affected Chinese Holstein calves. Data on birth weight, health status, and gestation length were collected from 4,584 IVP-derived Holstein calves and used for the analyses. Subsequently, 17 LOS-affected calves were identified based on birth weight. The data from these calves were statistically compared with that from 6 healthy calves in terms of organ weight, blood biochemical parameters, and pathological changes using general linear models and t-tests. The results showed that the average birth weight of IVP-derived calves was 40.79 ± 6.69 kg. The proportion of healthy calves was highest (86%) among calves with birth weight ranging from 33 to 47 kg, whereas it decreased to 18.4% when birth weight exceeded 61kg. In addition, birth weight was significantly affected by calving season, embryo cryopreservation method, oocyte retrieval season, calf sex, farm, and sire. The comparative analyses showed that LOS-affected calves had significantly greater body weight accompanied by bigger hearts, livers, spleens, lungs, kidneys, and tongues than healthy calves. The ALB of LOS group is significantly higher than the control group, while the glutathione of LOS group was significantly lower than the control. Histopathological examination revealed interstitial pneumonia in the lungs and inflammatory infiltration in the portal area of the liver in LOS-affected calves. To our knowledge, this is the first study establishing a quantitative phenotypic database for LOS diagnosis in Chinese IVP-derived Holstein calves. This study systematically reveals the coordinated characteristics of multi-organ hypertrophy, functional abnormalities, and pathological alterations in LOS calves. These findings provide detailed background information for LOS diagnosis in calves, management practices, and genetic selection for reduced incidence of LOS cases in Holstein calves. - Source: PubMed
Publication date: 2026/09/09
Qu LeiyuBrito Luiz FWang AoHang ZhengyuFang QianhaiMei ChengYang MingluZhang HailiangGao QingshanWang Yachun - The early developmental stages of fish exhibit the highest mortality and greatest environmental sensitivity throughout their life cycle. This period encompasses a series of crucial biological events, including morphogenesis, organ differentiation, and nutritional mode transition from fertilized eggs to newly hatched larvae. Although largemouth bass (Micropterus nigricans) is a commercially important fish species in China, the molecular regulatory mechanisms governing its endogenous nutritional stage remain largely unexplored. To elucidate the molecular basis of this critical period, we performed transcriptomic profiling across six consecutive developmental stages (Multicellular, Blastula, Gastrula, Neurula, Organogenesis, and 5 day post hatching larvae). Our results reveal stage-specific transcriptional programs: the multicellular-to-blastula transition is characterized by stage-specific enrichment of by cell cycle and DNA replication pathways, with MCM complex (mcm2-5) upregulation accelerating proliferation; the blastula-to-gastrula transition features activation of bmp4, fgfr2, and lft1 for germ layer induction; the neurula stage exhibits transcriptional bursts and enrichment of neural tube-related pathways; organogenesis involves simultaneous activation of focal adhesion (col1a1b, col4a5, tnc) and Wnt signaling (wnt1, wnt4, wnt3a) pathway; and 5 dph larvae show visual function maturation, with light transduction genes (gnat1, gnat2, gucy2f, pde6b) identified as hub genes. Mfuzz analysis further reveals sustained upregulation of Cluster 14 (igf2r、napin、vamp7、il1b、aco2) indicating functional maturation, while Cluster 29 (mcm10, espl1, cep152, cep44, cep295) confirms declining cell division activity. Collectively, this study provides a transcriptomic resource for understanding largemouth bass embryonic development and offers molecular insights for improving hatchery practices. - Source: PubMed
Publication date: 2026/08/31
Hua JixiangTao YifanSun HuiZhu TaideWang XiaoyiHuang XiaochenWang WenLu SiqiLu JianQiang Jun - Lysosomal storage disorders (LSDs) are intractable rare diseases caused by lysosomal dysfunction due mainly to defects in lysosomal enzyme genes. For many lysosomal enzymes to be transported correctly into lysosomes, their mannose-6-phosphate (M6P) labeling by GlcNAc-1 phosphotransferase is crucial. M6P-modified lysosomal enzymes are captured by M6P receptors and transported to lysosomes. The M6P-dependent pathway is utilized not only for newly synthesized lysosomal enzymes but also for the intracellular transport of exogenously administered lysosomal enzymes to lysosomes. In this study, we performed gene knockouts targeting the M6PR and IGF2R genes, which encode the M6P receptors. Cells with a double knockout of these genes secrete M6P-modified proteins into the culture supernatant double KO (dKO sup), and we investigated its potential for therapeutic application. I-cell disease (mucolipidosis II, ML-II) arises from GNPT deficiency and is a disorder in which dozens of lysosomal enzymes are deficient within the cell. Treating ML II cells with the dKO sup restored lysosomal enzyme activity, reduced inclusion bodies, and improved autophagic function. ML II patient-derived fibroblasts exhibited increased lysosomal enzyme activities, normalized morphology, and improved cryo-viability with the treatment. Niemann-Pick disease type C2 (NPC2) protein is not a lysosomal enzyme but functions cooperatively with NPC1 protein to mediate cholesterol transport in lysosomes. NPC2 deficiency causes NPC2, and the dKO sup restored the cellular function of the disease by supplementing the NPC2 protein. These results indicate that M6PR/IGF2R double-deficient cells provide a simple platform for supplying M6P-modified proteins that can be applied to the treatment of a broad range of LSDs. - Source: PubMed
Publication date: 2026/08/31
Fujita ToshiharuTerawaki SeigoMoriwaki TakahitoOtomo Takanobu