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Wählen Sie konfigurierbare Panels & Premixed-Kits - ODER - Kits für die zelluläre Signaltransduktion & MAPmates™
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Unser breites Angebot enthält Multiplex-Panels, für die Sie die Analyten auswählen können, die am besten für Ihre Anwendung geeignet sind. Unter einem separaten Register können Sie das Premixed-Cytokin-Format oder ein Singleplex-Kit wählen.
Kits für die zelluläre Signaltransduktion & MAPmates™
Wählen Sie gebrauchsfertige Kits zur Erforschung gesamter Signalwege oder Prozesse. Oder konfigurieren Sie Ihre eigenen Kits mit Singleplex MAPmates™.
Die folgenden MAPmates™ sollten nicht zusammen analysiert werden: -MAPmates™, die einen unterschiedlichen Assaypuffer erfordern. -Phosphospezifische und MAPmate™ Gesamtkombinationen wie Gesamt-GSK3β und Gesamt-GSK3β (Ser 9). -PanTyr und locusspezifische MAPmates™, z.B. Phospho-EGF-Rezeptor und Phospho-STAT1 (Tyr701). -Mehr als 1 Phospho-MAPmate™ für ein einziges Target (Akt, STAT3). -GAPDH und β-Tubulin können nicht mit Kits oder MAPmates™, die panTyr enthalten, analysiert werden.
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48-602MAG
Buffer Detection Kit for Magnetic Beads
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Use Anti-acetyl-c-Myc (Lys148) Antibody (Rabbit Polyclonal Antibody) validated in WB to detect acetyl-c-Myc (Lys148) also known as HLHe39, Proto-oncogene c-Myc, Transcription factor p64.
More>>Use Anti-acetyl-c-Myc (Lys148) Antibody (Rabbit Polyclonal Antibody) validated in WB to detect acetyl-c-Myc (Lys148) also known as HLHe39, Proto-oncogene c-Myc, Transcription factor p64. Less<<
Anti-acetyl-c-Myc (Lys148) Antibody: SDB (Sicherheitsdatenblätter), Analysenzertifikate und Qualitätszertifikate, Dossiers, Broschüren und andere verfügbare Dokumente.
c-Myc (bHLHe39) is a transcription factor that regulates the expression of multiple genes involved in apoptosis, cell growth, differentiation, and proliferation. Active c-Myc is coupled to the MAX protein via c-Myc’s C-terminal helix-loop-helix leucine zipper (bHLHLZ) domain. The c-Myc-MAX heterodimer also interacts with a number of other transcription-related proteins including TRRAP, p107 and Miz-1, and c-Myc-MAX may indirectly regulate histone acetylases involved in chromatin remodeling. c-Myc is itself acetylated on lysine 323 by GCN5, and on lysine 148 and 157 by p300/CBP. The significance of c-Myc acetylation is still under investigation; however, previous studies have suggested that HAT-dependent acetylation of c-Myc may regulate its turnover and stability. c-Myc may play a role in various cancers such as Burkitt’s lymphoma.
References
Product Information
Format
Affinity Purified
Control
Transfected HEK293 cell lysates
Presentation
Purified rabbit polyclonal in buffer containing 0.1 M Tris-Glycine (pH 7.4), 150 mM NaCl with 0.05% sodium azide.
Use Anti-acetyl-c-Myc (Lys148) Antibody (Rabbit Polyclonal Antibody) validated in WB to detect acetyl-c-Myc (Lys148) also known as HLHe39, Proto-oncogene c-Myc, Transcription factor p64.
Key Applications
Western Blotting
Application Notes
Peptide Inhibition Assay Analysis: 2 µg/mL from a representative lot blocked acetyl-c-Myc (Lys148) in HEK293T cells co-transfected with wildtype c-Myc and P300.
Peptide Inhibition Assay Analysis: A representative lot was used by an independent laboratory in HEK293T cells co-transfected with mouse wildtype c-Myc and P300. (Image courtesy of Dr. Ernest Martinez, Department of Biochemistry, University of California at Riverside.)
Biological Information
Immunogen
KLH-conjugated linear peptide corresponding to human c-Myc acetylated at Lys148.
Epitope
Acetylated Lys148
Concentration
Please refer to the Certificate of Analysis for the lot-specific concentration.
Host
Rabbit
Specificity
This antibody recognizes c-Myc acetylated at Lys148 in human and Lys149 in mouse.
Species Reactivity
Human
Mouse
Species Reactivity Note
Demonstrated to react with Mouse and Human. Predicted to react with Rat, Bovine, Canine, Rhesus Macaque, Chimpanzee, Sheep, and Porcine based on 100% sequence homology.
~58 kDa observed. Uniprot describes two isoforms at 49 and 51 kDa. Uncharacterized bands appear at ~13 and ~17 in some lysates.
Physicochemical Information
Dimensions
Materials Information
Toxicological Information
Safety Information according to GHS
Safety Information
Product Usage Statements
Quality Assurance
Evaluated by Western Blot in transfected HEK293 cell lysates.
Western Blot Analysis: 0.1 µg/mL of this antibody detected c-Myc on 10 µg of transfected HEK293 cell lysates.
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.
Using a screening strategy, we identified the tetratricopeptide repeat (TPR) motif protein, Tetratricopeptide repeat domain 5 (TTC5, also known as stress responsive activator of p300 or Strap) as required for the survival of human acute myeloid leukemia (AML) cells. TTC5 is a stress-inducible transcription cofactor known to interact directly with the histone acetyltransferase EP300 to augment the TP53 response. Knockdown (KD) of TTC5 induced apoptosis of both murine and human AML cells, with concomitant loss of clonogenic and leukemia-initiating potential; KD of EP300 elicited a similar phenotype. Consistent with the physical interaction of TTC5 and EP300, the onset of apoptosis following KD of either gene was preceded by reduced expression of BCL2 and increased expression of pro-apoptotic genes. Forced expression of BCL2 blocked apoptosis and partially rescued the clonogenic potential of AML cells following TTC5 KD. KD of both genes also led to the accumulation of MYC, an acetylation target of EP300, and the form of MYC that accumulated exhibited relative hypoacetylation at K148 and K157, residues targeted by EP300. In view of the ability of excess cellular MYC to sensitize cells to apoptosis, our data suggest a model whereby TTC5 and EP300 cooperate to prevent excessive accumulation of MYC in AML cells and their sensitization to cell death. They further reveal a hitherto unappreciated role for TTC5 in leukemic hematopoiesis.