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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 Proteins (2) and many more products for this protein.
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Human Polyclonal MAGEL2 Primary Antibody for EIA, IHC (p) - ABIN358645
De Smet, Lurquin, van der Bruggen, De Plaen, Brasseur, Boon: Sequence and expression pattern of the human MAGE2 gene. in Immunogenetics 1994
Show all 4 references for ABIN358645
Human Polyclonal MAGEL2 Primary Antibody for IHC (p), WB - ABIN390122
Lee, Kozlov, Hernandez, Chamberlain, Brannan, Stewart, Wevrick: Expression and imprinting of MAGEL2 suggest a role in Prader-willi syndrome and the homologous murine imprinting phenotype. in Human molecular genetics 2000
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A similar pro (show LEP Antibodies)gressive loss of leptin sensitivity caused by loss of MAGEL2 in children with Prader-Willi s (show LEP Antibodies)yndrome could ex (show POMC Antibodies)plain the delayed onset of increased appetite and weight gain in this complex disorder.
We find that MAGE-A2 (show MAGEA2 Antibodies) interacts with MDM2 (show MDM2 Antibodies) via the N-terminal p53 (show TP53 Antibodies)-binding pocket and the RING finger (show PCGF1 Antibodies) domain of MDM2 (show MDM2 Antibodies) 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 Antibodies)/7 activity, BCL2 (show BCL2 Antibodies)/BAX (show BAX Antibodies) 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 Antibodies) 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 Antibodies) acetylation at PML (show PML Antibodies)-nuclear bodies (NBs (show NBN Antibodies)) and with PMLIV-dependent activation of p53 (show TP53 Antibodies).
Report MAGEA1 (show MAGEA1 Antibodies)-A6 expression in sputum suggests presence of lung cancer cells or precancerous cells.
These data suggest that MAGEA2 is differentially expressed in HNSCC and functions, in part, through the p53 (show TP53 Antibodies) pathway by increasing cellular proliferation and abrogating cell cycle arrest.
Moreover, -712C>G and -708T>C had significant effects on MAGEL2 transcription and placental efficiency
Imprinting analysis showed that NDN (show NDN Antibodies) and MAGEL2 are paternally expressed in all tissues of pig where the genes were expressed as in human and mouse.
Normal leptin (show LEP Antibodies) responses were found in Magel2-null mice up to 4 weeks of age, but the proportion of leptin (show LEP Antibodies)-responsive POMC (show POMC Antibodies) 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 Antibodies) 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 Antibodies) and MAGE-G1 (show NDNL2 Antibodies) target both E2F1 (show E2F1 Antibodies) and p75 (show NGFR Antibodies) to regulate cell viability during brain development.
Inactivation of the mouse Magel2 gene results in growth abnormalities similar to Prader-Willi syndrome
The robust rhythmicity of Magel2 expression in the SCN (show SRI Antibodies) and the altered behavioral rhythmicity of null mice reveal Magel2 to be a clock-controlled circadian output gene whose disruption results in some of the phenotypes characteristic of PWS.
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