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Prader-Willi syndrome (PWS) is caused by the loss of expression of imprinted genes in chromosome 15q11-q13 region. Additionally we are shipping MAGE-Like 2 Antibodies (45) and MAGE-Like 2 Proteins (2) and many more products for this protein.
Immunohistochemistry using D2-40 monoclonal antibody (MAGE2) and anti-MITF1 increased detection of lymphovascular invasion in primary cutaneous melanoma.
A similar pro (show LEP ELISA Kits)gressive loss of leptin sensitivity caused by loss of MAGEL2 in children with Prader-Willi s (show LEP ELISA Kits)yndrome could ex (show POMC ELISA Kits)plain the delayed onset of increased appetite and weight gain in this complex disorder.
We find that MAGE-A2 interacts with MDM2 (show MDM2 ELISA Kits) via the N-terminal p53 (show TP53 ELISA Kits)-binding pocket and the RING finger (show PCGF1 ELISA Kits) domain of MDM2 (show MDM2 ELISA Kits) that is required for homo/hetero-dimerization and for E2 ligase interaction.
Truncating Mutations of MAGEL2, a Gene within the Prader-Willi Locus, Are Responsible for Severe Arthrogryposis.
Consistent with increased cell death, the induced loss of MAGEA2 expression correlated with increased caspase 3 (show CASP3 ELISA Kits)/7 activity, BCL2 (show BCL2 ELISA Kits)/BAX (show BAX ELISA Kits) ratio and TUNEL signal.
MAGEA2 has a critical role in the development of tamoxifen-resistant breast cancer
MAGEL2 is a new gene causing complex autism spectrum disorder and MAGEL2 loss of function can contribute to several aspects of the Prader-Willi syndrome phenotype.
These findings provide a cellular and molecular function for MAGE-L2-TRIM27 (show RFP ELISA Kits) in retrograde transport, including an unappreciated role of K63-linked ubiquitination and identification of an activating signal of the WASH regulatory complex.
MageA2 interferes with p53 (show TP53 ELISA Kits) acetylation at PML (show PML ELISA Kits)-nuclear bodies (NBs (show NBN ELISA Kits)) and with PMLIV-dependent activation of p53 (show TP53 ELISA Kits).
Report MAGEA1 (show MAGEA1 ELISA Kits)-A6 expression in sputum suggests presence of lung cancer cells or precancerous cells.
Moreover, -712C>G and -708T>C had significant effects on MAGEL2 transcription and placental efficiency
Imprinting analysis showed that NDN (show NDN ELISA Kits) and MAGEL2 are paternally expressed in all tissues of pig where the genes were expressed as in human and mouse.
Magel2 knockout mice displayed altered social phenotype and a lack of preference for social novelty.
these findings suggest that a loss of Magel2 leads to the disruption of hypothalamic feeding circuits, an effect that appears to be independent of the neurodevelopmental effects of leptin (show LEP ELISA Kits) and ghrelin (show GHRL ELISA Kits) and likely involves a direct neurotrophic effect of Magel2.
Normal leptin (show LEP ELISA Kits) responses were found in Magel2-null mice up to 4 weeks of age, but the proportion of leptin (show LEP ELISA Kits)-responsive POMC (show POMC ELISA Kits) neurons was reduced in 6-week-old Magel2-null mice.
Magel2 inactivation induces a deficit in social recognition and social interaction and a reduced learning ability in adult male mice.
This neural defect, together with increased fat mass, blunted circadian rhythm, and growth hormone (show GH1 ELISA Kits) response pathway defects that are also linked to loss of MAGEL2, could contribute to the hyperphagia and obesity that are hallmarks of this disorder.
This study demonstrated that Magel2-null mice have abnormalities of hypothalamic endocrine axes that recapitulate phenotypes in Prader-Willi syndrome.
Magel2-deficient mouse with 50% neonatal mortality had an altered onset of suckling activity and subsequent impaired feeding.
Magel2 gene is imprinted, with preferential expression from the paternal allele in mouse and human.
role of the circadian rhythm output gene Magel2 in brain structure and behavior
necdin (show NDN ELISA Kits) and MAGE-G1 (show NDNL2 ELISA Kits) target both E2F1 (show E2F1 ELISA Kits) and p75 (show NGFR ELISA Kits) to regulate cell viability during brain development.
This gene is a member of the MAGEA gene family. The members of this family encode proteins with 50 to 80% sequence identity to each other. The promoters and first exons of the MAGEA genes show considerable variability, suggesting that the existence of this gene family enables the same function to be expressed under different transcriptional controls. The MAGEA genes are clustered at chromosomal location Xq28. They have been implicated in some hereditary disorders, such as dyskeratosis congenita. This gene has two identical copies at different loci. Alternatively spliced transcript variants encoding the same protein have been identified for this gene.
, MAGE-like protein 2
, necdin-like protein 1
, protein nM15
, melanoma antigen-like gene 2
, melanoma antigen, family L, 2
, MAGE-2 antigen
, cancer/testis antigen 1.2
, cancer/testis antigen family 1, member 2
, melanoma antigen 2
, melanoma-associated antigen 2
, necdin-like 1
, protein nS7