Xeroderma pigmentosum group A-complementing protein (XPA) or DNA repair protein complementing XP-A cells human excision repair protein. XPA encodes a hydrophilic metalloprotein. It displays a C4 zinc finger motif, a central globular domain and has disordered regions in the N and C-terminus. The gene XPA is localized in human chromosome 9q22.33.
Specificity
Anti-XPA (C-terminal) specifically recognizes human XPA.
Immunogen
synthetic peptide corresponding to amino acids 257-273 of human XPA, conjugated to KLH via an N-terminal added cysteine residue. The immunizing peptide differs from the mouse and rat sequences by one amino acid.
Application
Anti-XPA (C-terminal) antibody produced in rabbit has been used in immunolabeling and immunoblotting.
Biochem/physiol Actions
Xeroderma pigmentosum group A-complementing protein (XPA) interacts with nucleotide excision repair (NER) subunits, such as replication protein A (RPA), excision repair complementing 1 protein (ERCC1), and transcription factor II (TFIIH). However, it is widely accepted that the Xeroderma pigmentosum group C-complementing protein (XPC)-human Rad23 homolog (hHR23B) complex recognizes the DNA damage-induced helical distortion. After this, the transcription factor IIH (TFIIH), XPA (possibly in its homodimeric form), and replication protein A (RPA) arrive sequentially at the site of damage. XPA interacts directly with DNA via the zinc finger motif. RPA coordinates with XPA in the positioning in the nucleotide excision repair (NER) bubble. Defects in the excision repair leads to photosensitivity syndrome called xeroderma pigmentosum (XP).
Physical form
Solution in 0.01 M phosphate buffered saline, pH 7.4, containing 15 mM sodium azide.
Storage and Stability
For continuous use, store at 2-8 °C for up to one month. For extended storage, freeze in working aliquots. Repeated freezing and thawing, or storage in “frost-free” freezers, is not recommended. If slight turbidity occurs upon prolonged storage, clarify the solution by centrifugation before use. Working dilutions should be discarded if not used within 12 hours.
Disclaimer
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.
Xeroderma pigmentosum (XP) is an inherited disease in which cells from patients exhibit defects in nucleotide excision repair (NER). XP proteins A-G are crucial in the processes of DNA damage recognition and incision, and patients with XP can carry mutations
Effects of tryptophan and portocaval anastomosis on activity and brain tryptophan metabolism [proceedings].
D L Bloxam et al.
British journal of pharmacology, 60(2), 277P-277P (1977-06-01)
Hyperpigmentation is a key feature in a variety of inherited and acquired syndromes. Nonetheless, determining the exact diagnosis only on the clinical phenotype can be challenging, and a detailed search for associated symptoms is often of crucial importance. As pigmentation
The XPA protein functions together with the single-stranded DNA (ssDNA) binding protein RPA as the central scaffold to ensure proper positioning of repair factors in multi-protein nucleotide excision repair (NER) machinery. We previously determined the structure of a short motif
International journal of molecular sciences, 21(6) (2020-04-03)
The nucleotide excision repair (NER) pathway is activated in response to a broad spectrum of DNA lesions, including bulky lesions induced by platinum-based chemotherapeutic agents. Expression levels of NER factors and resistance to chemotherapy has been examined with some suggestion
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