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Rabbit Anti-APEX2/PE-Cy5.5 Conjugated antibody (bs-6587R-PE-Cy5.5)
訂購熱線:400-901-9800
訂購郵箱:sales@bioss.com.cn
訂購QQ:  400-901-9800
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說 明 書: 100ul  
100ul/2980.00元
大包裝/詢價
產(chǎn)品編號 bs-6587R-PE-Cy5.5
英文名稱 Rabbit Anti-APEX2/PE-Cy5.5 Conjugated antibody
中文名稱 PE-Cy5.5標記的嘌呤嘧啶核酸內(nèi)切酶2抗體
別    名 AP endonuclease 2; AP endonuclease XTH2; APE 2; APE2; APEX 2; APEX L2; APEX nuclease (apurinic/apyrimidinic endonuclease) 2; APEX Nuclease 2; APEX nuclease like 2; APEXL 2; APEXL2; Apurinic apyrimidinic endonuclease 2; Apurinic/apyrimidinic endonuclease 2; Apurinic/apyrimidinic endonuclease like 2; C430040P13Rik; DNA (apurinic or apyrimidinic site) lyase 2; XTH 2; XTH2; APEX2_HUMAN.  
規(guī)格價格 100ul/2980元 購買        大包裝/詢價
說 明 書 100ul  
研究領(lǐng)域 細胞生物  染色質(zhì)和核信號  
抗體來源 Rabbit
克隆類型 Polyclonal
交叉反應 Mouse, Rat,  (predicted: Human, Dog, Cow, )
產(chǎn)品應用 IF=1:50-200 
not yet tested in other applications.
optimal dilutions/concentrations should be determined by the end user.
分 子 量 57kDa
性    狀 Lyophilized or Liquid
濃    度 1mg/ml
免 疫 原 KLH conjugated synthetic peptide derived from human APEX2
亞    型 IgG
純化方法 affinity purified by Protein A
儲 存 液 0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol.
保存條件 Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. The lyophilized antibody is stable at room temperature for at least one month and for greater than a year when kept at -20°C. When reconstituted in sterile pH 7.4 0.01M PBS or diluent of antibody the antibody is stable for at least two weeks at 2-4 °C.
產(chǎn)品介紹 background:
Apurinic/apyrimidinic (AP) sites occur frequently in DNA molecules by spontaneous hydrolysis, by DNA damaging agents or by DNA glycosylases that remove specific abnormal bases. AP sites are pre-mutagenic lesions that can prevent normal DNA replication so the cell contains systems to identify and repair such sites. Class II AP endonucleases cleave the phosphodiester backbone 5' to the AP site. This gene encodes a protein shown to have a weak class II AP endonuclease activity. Most of the encoded protein is located in the nucleus but some is also present in mitochondria. This protein may play an important role in both nuclear and mitochondrial base excision repair (BER).

Function:
Function as a weak apurinic/apyrimidinic (AP) endodeoxyribonuclease in the DNA base excision repair (BER) pathway of DNA lesions induced by oxidative and alkylating agents. Initiates repair of AP sites in DNA by catalyzing hydrolytic incision of the phosphodiester backbone immediately adjacent to the damage, generating a single-strand break with 5'-deoxyribose phosphate and 3'-hydroxyl ends. Displays also double-stranded DNA 3'-5' exonuclease, 3'-phosphodiesterase activities. Shows robust 3'-5' exonuclease activity on 3'-recessed heteroduplex DNA and is able to remove mismatched nucleotides preferentially. Shows fairly strong 3'-phosphodiesterase activity involved in the removal of 3'-damaged termini formed in DNA by oxidative agents. In the nucleus functions in the PCNA-dependent BER pathway. Required for somatic hypermutation (SHM) and DNA cleavage step of class switch recombination (CSR) of immunoglobulin genes. Required for proper cell cycle progression during proliferation of peripheral lymphocytes.

Subunit:
Interacts with PCNA; this interaction is triggered by reactive oxygen species and increased by misincorporation of uracil in nuclear DNA.

Subcellular Location:
Nucleus. Cytoplasm. Mitochondrion (Probable). Note=Together with PCNA, is redistributed in discrete nuclear foci in presence of oxidative DNA damaging agents.

Tissue Specificity:
Highly expressed in brain and kidney. Weakly expressed in the fetal brain.

Similarity:
Belongs to the DNA repair enzymes AP/ExoA family.

Database links:

Entrez Gene:  Human

Entrez Gene: 77622 Mouse

Entrez Gene: 289662 Rat

Omim: 300773 Human

SwissProt: Q9UBZ4 Human

SwissProt: Q68G58 Mouse

Unigene: 659558 Human

Unigene: 440275 Mouse



Important Note:
This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.
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