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Prader-Willi syndrome (PWS) is caused by the loss of expression of imprinted genes in chromosome 15q11-q13 region. Zusätzlich bieten wir Ihnen MAGE-Like 2 Proteine (2) und viele weitere Produktgruppen zu diesem Protein an.
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Human Polyclonal MAGEL2 Primary Antibody für 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
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Human Polyclonal MAGEL2 Primary Antibody für 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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Immunohistochemistry using D2-40 monoclonal antibody (MAGE2) and anti-MITF1 increased detection of lymphovascular invasion in primary cutaneous melanoma.
A similar pro (zeige LEP Antikörper)gressive loss of leptin sensitivity caused by loss of MAGEL2 in children with Prader-Willi s (zeige LEP Antikörper)yndrome could ex (zeige POMC Antikörper)plain the delayed onset of increased appetite and weight gain in this complex disorder.
We find that MAGE-A2 (zeige MAGEA2 Antikörper) interacts with MDM2 (zeige MDM2 Antikörper) via the N-terminal p53 (zeige TP53 Antikörper)-binding pocket and the RING finger (zeige PCGF1 Antikörper) domain of MDM2 (zeige MDM2 Antikörper) 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 (zeige CASP3 Antikörper)/7 activity, BCL2 (zeige BCL2 Antikörper)/BAX (zeige BAX Antikörper) 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 (zeige RFP Antikörper) 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 (zeige TP53 Antikörper) acetylation at PML (zeige PML Antikörper)-nuclear bodies (NBs (zeige NBN Antikörper)) and with PMLIV-dependent activation of p53 (zeige TP53 Antikörper).
Report MAGEA1 (zeige MAGEA1 Antikörper)-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 (zeige NDN Antikörper) and MAGEL2 are paternally expressed in all tissues of pig where the genes were expressed as in human and mouse.
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 (zeige LEP Antikörper) and ghrelin (zeige GHRL Antikörper) and likely involves a direct neurotrophic effect of Magel2.
Normal leptin (zeige LEP Antikörper) responses were found in Magel2-null mice up to 4 weeks of age, but the proportion of leptin (zeige LEP Antikörper)-responsive POMC (zeige POMC Antikörper) 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 (zeige GH1 PLURAL_@26348@) 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 (zeige NDN Antikörper) and MAGE-G1 (zeige NDNL2 Antikörper) target both E2F1 (zeige E2F1 Antikörper) and p75 (zeige NGFR Antikörper) to regulate cell viability during brain development.
Inactivation of the mouse Magel2 gene results in growth abnormalities similar to Prader-Willi syndrome
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