Vergleich

TBP (TATA box binding protein)

ArtNr 18-003-43056
Hersteller GENWAY
Menge 0.1 mg
Kategorie
Typ Antibody
Applikationen WB
Specific against other
ECLASS 10.1 32160702
ECLASS 11.0 32160702
UNSPSC 12352203
Alias GWB-96B386
Similar products 18-003-43056
Lieferbar
Genway ID:
GWB-96B386
Dilution:
2. 5ug/ml
Immunogen:
FSSGKMVCTGAKSEEQSRLAARKYARVVQKLGFPAKFLDFKIQNMVGSCD
Appearance:
Lyophilized powder.
Handling:
Add 100ul of distilled water to this antibody before use.
ELISA Titre:
1:62500
Note:
Suggested starting concentrations are provided. Optimal dilutions should be determined by end-user. Differences in calculated versus apparent molecular weight may be due to post-translational modifications or protein hydrophobicity. 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.
Function:
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.
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. Interacts with GPBP1 (By similarity).
Subcellular Location:
Nucleus.
Polymorphism:
The poly-Gln region of TBP is highly polymorphic (25 to 42 repeats) in normal individuals and is expanded to about 47-63 repeats in spinocerebellar ataxia 17 (SCA17) patients.
Disease:
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:
Belongs to the TBP family. Summary: 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 protein is 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. Reid. S. J. . et al. . (2004) Brain Res. Mol. Brain Res. 125 (1-2). 120-128. Product Protocol: To see this product used in a peer reviewed journal click the following link: LCAT-null mice develop improved hepatic insulin sensitivity through altered regulation of transcription factors and suppressors of cytokine signaling

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Menge: 0.1 mg
Lieferbar: In stock
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