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Mouse Monoclonal TFIIH p89 antibody (STJ98562)
Supplier: St John’s Laboratory Ltd.
Recommended applications: WB
Recommended dilution: WB 1:1000-1:2000
Recommended protocols: check protocols
Click or hover above images to see image description for TFIIH p89 Monoclonal Antibody.
Check alternative names for the antibodyExpand
ERCC3 antibody, XPB antibody, XPBC antibody,|Basic transcription factor 2 89 kDa subunit antibody|BTF 2 antibody|BTF2 antibody|BTF2 p89 antibody|DNA excision repair protein ERCC-3 antibody|DNA repair protein complementing XP-B cells antibody|ERCC 3 antibody|ercc3 antibody|ERCC3_HUMAN antibody|Excision Repair Cross-complementing Rodent Repair deficiency complementation Group 3 antibody|GTF2H antibody|RAD 25 antibody|RAD25 antibody|TFIIH 89 kDa subunit antibody|TFIIH antibody|TFIIH basal transcription factor complex 89 kDa subunit antibody|TFIIH basal transcription factor complex helicase XPB subunit antibody|TFIIH p89 antibody|Xeroderma pigmentosum group B-complementing protein antibody|Anti-XPB antibody (ab27317)
SCBT cat No: To be updated
TFIIH p89 Monoclonal Antibody
|Catalogue No.|| |
Human, Mouse, Rat, Cow, Dog
TFIIH p89 Monoclonal Antibody detects endogenous levels of TFIIH p89 protein.
Purified recombinant human TFIIH p89 (C-terminus) protein fragments expressed in Ecoli
|Recommended dilution|| |
TFIIH p89 Antibody was tube-contained. Purified in buffer containing 0.1M Tris-Glycine (pH 7.4, 150 mM NaCl) with 0.2% sodium azide, 50% glycerol.
TFIIH p89 Antibody was purified using affinity purification.
-20 Celsius degree. Avoid repeated freeze/thaw cycles.
|Alternative antibody names|| |
TFIIH basal transcription factor complex helicase XPB subunit antibody, Basic transcription factor 2 89 kDa subunit antibody, BTF2 p89 antibody, DNA excision repair protein ERCC-3 antibody, DNA repair protein complementing XP-B cells antibody, TFIIH basal transcription factor complex 89 kDa subunit antibody, TFIIH 89 kDa subunit antibody, TFIIH p89 antibody, Xeroderma pigmentosum group B-complementing protein antibody
|Protein names|| |
TFIIH basal transcription factor complex helicase XPB subunit , Basic transcription factor 2 89 kDa subunit , BTF2 p89 , DNA excision repair protein ERCC-3 , DNA repair protein complementing XP-B cells , TFIIH basal transcription factor complex 89 kDa subunit , TFIIH 89 kDa subunit , TFIIH p89 , Xeroderma pigmentosum group B-complementing protein
|Protein function|| |
ATP-dependent 3′-5′ DNA helicase, component of the core-TFIIH basal transcription factor, involved in nucleotide excision repair (NER) of DNA and, when complexed to CAK, in RNA transcription by RNA polymerase II. Acts by opening DNA either around the RNA transcription start site or the DNA damage. / ATP + H2O = ADP + phosphate.
|Involvement in disease|| |
Xeroderma pigmentosum complementation group B (XP-B) [MIM:610651]: An autosomal recessive pigmentary skin disorder characterized by solar hypersensitivity of the skin, high predisposition for developing cancers on areas exposed to sunlight and, in some cases, neurological abnormalities. The skin develops marked freckling and other pigmentation abnormalities. Some XP-B patients present features of Cockayne syndrome, including cachectic dwarfism, pigmentary retinopathy, ataxia, decreased nerve conduction velocities. The phenotype combining xeroderma pigmentosum and Cockayne syndrome traits is referred to as XP-CS complex. . Note: The disease is caused by mutations affecting the gene represented in this entry.; Trichothiodystrophy 2, photosensitive (TTD2) [MIM:616390]: A form of trichothiodystrophy, an autosomal recessive disease characterized by sulfur-deficient brittle hair and multisystem variable abnormalities. The spectrum of clinical features varies from mild disease with only hair involvement to severe disease with cutaneous, neurologic and profound developmental defects. Ichthyosis, intellectual and developmental disabilities, decreased fertility, abnormal characteristics at birth, ocular abnormalities, short stature, and infections are common manifestations. There are both photosensitive and non-photosensitive forms of the disorder. . Note: The disease is caused by mutations affecting the gene represented in this entry.
|Protein sequence and domain|| |
Belongs to the helicase family. RAD25/XPB subfamily. / Contains 1 helicase ATP-binding domain. / Contains 1 helicase C-terminal domain.
|Protein cellular localization|| |
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St John’s Laboratory Ltd.
|Product type|| |
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