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Wählen Sie konfigurierbare Panels & Premixed-Kits - ODER - Kits für die zelluläre Signaltransduktion & MAPmates™
Konfigurieren Sie Ihre MILLIPLEX® MAP-Kits und lassen sich den Preis anzeigen.
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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
1 Kit
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Anti-TATA-Binding-Protein Antibody is a Mouse Monoclonal Antibody for detection of TATA-Binding-Protein also known as TBP & has been validated in WB, ICC & IHC.
More>>Anti-TATA-Binding-Protein Antibody is a Mouse Monoclonal Antibody for detection of TATA-Binding-Protein also known as TBP & has been validated in WB, ICC & IHC. Less<<
Anti-TATA-Binding-Protein Antibody: SDB (Sicherheitsdatenblätter), Analysenzertifikate und Qualitätszertifikate, Dossiers, Broschüren und andere verfügbare Dokumente.
Anti-TATA-Binding-Protein Antibody is a Mouse Monoclonal Antibody for detection of TATA-Binding-Protein also known as TBP & has been validated in WB, ICC & IHC.
Key Applications
Western Blotting
Immunocytochemistry
Immunohistochemistry
Application Notes
Western blot: 1:1,000-1:5,000 on endogenous and recombinant protein.
Immunohistochemistry: 1:1,000-1:5,000
Immunocytochemistry: 1:1,000-1:5,000
Immunoprecipitation
ELISA: 1:1,000-1:5,000
Optimal working dilutions must be determined by the end user.
Biological Information
Immunogen
Full length recombinant human TBP.
Epitope
a.a. 1-18
Host
Mouse
Specificity
Recognizes TATA-binding-protein (TBP). Recognizes an epitope from the first 18 amino acids of human TBP.
Isotype
IgG1
Species Reactivity
Chicken
Human
Mouse
Xenopus
Fish
Species Reactivity Note
Human, mouse, chicken, xenopus and zebrafish. Does not react with Drososphila. Reactivity with other species has not been confirmed.
Initiation of transcription by RNA polymerase II requires the activities of more than 70 polypeptides. The protein that coordinates these activities is transcription factor IID (TFIID), which binds to the core promoter to position the polymerase properly, serves as the scaffold for assembly of the remainder of the transcription complex, and acts as a channel for regulatory signals. TFIID is composed of the TATA-binding protein (TBP) and a group of evolutionarily conserved proteins known as TBP-associated factors or TAFs. TAFs may participate in basal transcription, serve as coactivators, function in promoter recognition or modify general transcription factors (GTFs) to facilitate complex assembly and transcription initiation. This gene encodes TBP, the TATA-binding protein. A distinctive feature of TBP is a long string of glutamines in the N-terminal. This region of the protein modulates the DNA binding activity of the C terminus, and modulation of DNA binding affects the rate of transcription complex formation and initiation of transcription. Mutations that expand the number of CAG repeats encoding this polyglutamine tract, and thus increase the length of the polyglutamine string, are associated with spinocerebellar ataxia 17, a neurodegenerative disorder classified as a polyglutamine disease.
FUNCTION: SwissProt: P20226 # General transcription factor that functions at the core of the DNA-binding multiprotein factor TFIID. Binding of TFIID to the TATA box is the initial transcriptional step of the pre- initiation complex (PIC), playing a role in the activation of eukaryotic genes transcribed by RNA polymerase II. SIZE: 339 amino acids; 37698 Da SUBUNIT: Belongs to the TFIID complex together with the TBP- associated factors (TAFs). Component of the transcription factor SL1/TIFIB complex, composed of TBP and at least TAF1A, TAF1B TAF1C, and TAF3. Binds DNA as monomer. Interacts with TAFs, TFIIB, NCOA6, DRAP1, DR1 and ELF3. Interacts with SPIB, SNAPC1, SNAPC2 and SNAPC4. Interacts with HIV-1 Tat. Interacts with UTF1 which acts as a coactivator of ATF2 transcriptional activity. SUBCELLULAR LOCATION: Nucleus. DISEASE: SwissProt: P20226 # Defects in TBP are the cause of spinocerebellar ataxia 17 (SCA17) [MIM:607136]. Spinocerebellar ataxia is a clinically and genetically heterogeneous group of autosomal dominant cerebellar ataxias (ADCA). Patients show progressive incoordination of gait and often poor coordination of hands, speech and eye movements. Spinocerebellar ataxia is caused by degeneration of the cerebellum with variable involvement of the brainstem and spinal cord. The molecular defect in SCA17 is the expansion of a CAG repeat in the coding region of TBP. Longer expansions result in earlier onset and more severe clinical manifestations of the disease. SIMILARITY: SwissProt: P20226 ## Belongs to the TBP family.
Molecular Weight
~42 kDa
Physicochemical Information
Dimensions
Materials Information
Toxicological Information
Safety Information according to GHS
Safety Information
Product Usage Statements
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
Maintain at -20°C in undiluted aliquots for up to 6 months after date of receipt. Avoid repeated freeze/thaw cycles.
Angelman syndrome (AS) is a severe neurodevelopmental disorder caused by maternal deficiency of the imprinted gene UBE3A. Individuals with AS suffer from intellectual disability, speech impairment, and motor dysfunction. Currently there is no cure for the disease. Here, we evaluated the phenotypic effect of activating the silenced paternal allele of Ube3a by depleting its antisense RNA Ube3a-ATS in mice. Premature termination of Ube3a-ATS by poly(A) cassette insertion activates expression of Ube3a from the paternal chromosome, and ameliorates many disease-related symptoms in the AS mouse model, including motor coordination defects, cognitive deficit, and impaired long-term potentiation. Studies on the imprinting mechanism of Ube3a revealed a pattern of biallelic transcription initiation with suppressed elongation of paternal Ube3a, implicating transcriptional collision between sense and antisense polymerases. These studies demonstrate the feasibility and utility of unsilencing the paternal copy of Ube3a via targeting Ube3a-ATS as a treatment for Angelman syndrome.
An RNA interference screen identifies the Deubiquitinase STAMBPL1 as a critical regulator of human T-cell leukemia virus type 1 tax nuclear export and NF-κB activation. Lavorgna, A; Harhaj, EW Journal of virology
86
3357-69
2011
The human T-cell leukemia virus type 1 (HTLV-1) Tax oncoprotein actively shuttles between the nucleus, where it interacts with transcriptional and splicing regulatory proteins, and the cytoplasm, where it activates NF-κB. Posttranslational modifications of Tax such as ubiquitination regulate its subcellular localization and hence its function; however, the regulation of Tax trafficking and NF-κB activation by host factors is poorly understood. By screening a deubiquitinating (DUB) enzyme small interfering RNA (siRNA) library, we identified the metalloprotease STAM-binding protein-like 1 (STAMBPL1) as a positive regulator of Tax-mediated NF-κB activation. Overexpression of wild-type STAMBPL1, but not a catalytically inactive mutant, enhanced Tax-mediated NF-κB activation, whereas silencing of STAMBPL1 with siRNA impaired Tax activation of both the canonical and noncanonical NF-κB signaling pathways. STAMBPL1 regulated Tax-induced NF-κB signaling indirectly by controlling Tax nuclear/cytoplasmic transport and was required for DNA damage-induced Tax nuclear export. Together, these results reveal that the deubiquitinase STAMBPL1 is a key regulator of Tax trafficking and function.
