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16-170
Sigma-AldrichAnti-Myc Tag Antibody, clone 9E10, biotin conjugate
Anti-Myc Tag Antibody, clone 9E10, biotin conjugate detects level of Myc Tag & has been published & validated for use in WB & IC.
More>>Anti-Myc Tag Antibody, clone 9E10, biotin conjugate detects level of Myc Tag & has been published & validated for use in WB & IC. Less<<
SDB (Sicherheitsdatenblätter), Analysenzertifikate und Qualitätszertifikate, Dossiers, Broschüren und andere verfügbare Dokumente.
The protein encoded by this gene is a multifunctional, nuclear phosphoprotein that plays a role in cell cycle progression, apoptosis and cellular transformation. It functions as a transcription factor that regulates transcription of specific target genes. Mutations, overexpression, rearrangement and translocation of this gene have been associated with a variety of hematopoietic tumors, leukemias and lymphomas, including Burkitt lymphoma. There is evidence to show that alternative translation initiations from an upstream, in-frame non-AUG (CUG) and a downstream AUG start site result in the production of two isoforms with distinct N-termini. The synthesis of non-AUG initiated protein is suppressed in Burkitt's lymphomas, suggesting its importance in the normal function of this gene.
FUNCTION: SwissProt: P01106 # Participates in the regulation of gene transcription. Binds DNA both in a non-specific manner and also specifically to recognizes the core sequence 5'-CAC[GA]TG-3'. Seems to activate the transcription of growth-related genes. SIZE: 439 amino acids; 48804 Da SUBUNIT: Efficient DNA binding requires dimerization with another bHLH protein. Binds DNA as a heterodimer with MAX. Interacts with TAF1C and SPAG9. Interacts with PARP10. Interacts with JARID1A and JARID1B. SUBCELLULAR LOCATION: Nucleus. PTM: Phosphorylated by PRKDC. DISEASE: SwissProt: P01106 # Overexpression of MYC is implicated in the etiology of a variety of hematopoietic tumors. & A chromosomal aberration involving MYC may be a cause of a form of B-cell chronic lymphocytic leukemia. Translocation t(8;12)(q24;q22) with BTG1. SIMILARITY: SwissProt: P01106 ## Contains 1 basic helix-loop-helix (bHLH) domain.
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Quality Assurance
routinely evaluated by immunoblot in HeLa nuclear extract and myc-tagged recombinant protein
Usage Statement
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
Storage and Shipping Information
Storage Conditions
1 year at 4°C
Packaging Information
Material Size
200 µg
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Supplemental Information
Specifications
Global Trade Item Number
Bestellnummer
GTIN
16-170
04053252740046
Documentation
Anti-Myc Tag Antibody, clone 9E10, biotin conjugate SDB
Delineating the molecular basis of synapse development is crucial for understanding brain function. Cocultures of neurons with transfected fibroblasts have demonstrated the synapse-promoting activity of candidate molecules. Here, we performed an unbiased expression screen for synaptogenic proteins in the coculture assay using custom-made cDNA libraries. Reisolation of NGL-3/LRRC4B and neuroligin-2 accounts for a minority of positive clones, indicating that current understanding of mammalian synaptogenic proteins is incomplete. We identify LRRTM1 as a transmembrane protein that induces presynaptic differentiation in contacting axons. All four LRRTM family members exhibit synaptogenic activity, LRRTMs localize to excitatory synapses, and artificially induced clustering of LRRTMs mediates postsynaptic differentiation. We generate LRRTM1(-/-) mice and reveal altered distribution of the vesicular glutamate transporter VGLUT1, confirming an in vivo synaptic function. These results suggest a prevalence of LRR domain proteins in trans-synaptic signaling and provide a cellular basis for the reported linkage of LRRTM1 to handedness and schizophrenia.
Signals from the extracellular matrix are essential for the survival of many cell types. Dominant-negative mutants of two members of Rho family GTPases, Rac1 and Cdc42, mimic the loss of anchorage in primary mouse fibroblasts and are potent inducers of apoptosis. This pathway of cell death requires the activation of both the p53 tumor suppressor and the extracellular signal-regulated mitogen-activated protein kinases (Erks). Here we characterize the proapoptotic Erk signal and show that it differs from the classically observed survival-promoting one by the intensity of the kinase activation. The disappearance of the GTP-bound forms of Rac1 and Cdc42 gives rise to proapoptotic, moderate activation of the Raf-MEK-Erk cascade via a signaling pathway involving the kinases phosphatidlyinositol 3-kinase and Akt. Moreover, concomitant activation of p53 and inhibition of Akt are both necessary and sufficient to signal anoikis in primary fibroblasts. Our data demonstrate that the GTPases of the Rho family control three major components of cellular signal transduction, namely, p53, Akt, and Erks, which collaborate in the induction of apoptosis due to the loss of anchorage.
Six monoclonal antibodies have been isolated from mice immunized with synthetic peptide immunogens whose sequences are derived from that of the human c-myc gene product. Five of these antibodies precipitate p62c-myc from human cells, and three of these five also recognize the mouse c-myc gene product. None of the antibodies sees the chicken p110gag-myc protein. All six antibodies recognize immunoblotted p62c-myc. These reagents also provide the basis for an immunoblotting assay by which to quantitate p62c-myc in cells.
Millipore’s Anti-myc antibodies demonstrate specificity against the myc-tag. See below for related products for myc. All Millipore antibodies are based on the expertise of Upstate & Chemicon. Weitere Informationen >>