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Rabbit Anti-PRMT5/BF594 Conjugated antibody (bs-6992R-BF594)
訂購熱線:400-901-9800
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訂購QQ:  400-901-9800
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說 明 書: 100ul  
100ul/2980.00元
大包裝/詢價(jià)
產(chǎn)品編號(hào) bs-6992R-BF594
英文名稱 Rabbit Anti-PRMT5/BF594 Conjugated antibody
中文名稱 BF594標(biāo)記的組蛋白精氨酸甲基轉(zhuǎn)移酶5抗體
別    名 72 kDa ICln binding protein; 72 kDa ICln-binding protein; ANM5_HUMAN; Histone-arginine N-methyltransferase PRMT5; HMT1 hnRNP methyltransferase like 5; HOMOLOG OF; SKB1; HRMT1L5; IBP72; Jak-binding protein 1; JBP 1; JBP1; PRMT 5; PRMT5; Protein arginine methyltransferase 5; Protein arginine N methyltransferase 5; Protein arginine N-methyltransferase 5; S. POMBE; S. POMBE HOMOLOG OF; SKB1; SHK1 KINASE BINDING PROTEIN 1; Shk1 kinase binding protein 1 homolog; SHK1 KINASE-BINDING PROTEIN 1; Shk1 kinase-binding protein 1 homolog; SKB 1; SKB1; SKB1 homolog; SKB1: SKB1 homolog (S. pombe); SKB1Hs.  
規(guī)格價(jià)格 100ul/2980元 購買        大包裝/詢價(jià)
說 明 書 100ul  
研究領(lǐng)域 細(xì)胞生物  染色質(zhì)和核信號(hào)  信號(hào)轉(zhuǎn)導(dǎo)  表觀遺傳學(xué)  
抗體來源 Rabbit
克隆類型 Polyclonal
交叉反應(yīng) Human, Mouse,  (predicted: Rat, Dog, Pig, Cow, Horse, Rabbit, )
產(chǎn)品應(yīng)用 IF=1:50-200 
not yet tested in other applications.
optimal dilutions/concentrations should be determined by the end user.
分 子 量 70kDa
性    狀 Lyophilized or Liquid
濃    度 1mg/ml
免 疫 原 KLH conjugated synthetic peptide derived from human PRMT5
亞    型 IgG
純化方法 affinity purified by Protein A
儲(chǔ) 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:
Arginine methyltransferase that can both catalyze the formation of omega-N monomethylarginine (MMA) and symmetrical dimethylarginine (sDMA), with a preference for the formation of MMA. Specifically mediates the symmetrical dimethylation of arginine residues in the small nuclear ribonucleoproteins Sm D1 (SNRPD1) and Sm D3 (SNRPD3); such methylation being required for the assembly and biogenesis of snRNP core particles. Methylates SUPT5H. Mono- and dimethylates arginine residues of myelin basic protein (MBP) in vitro. Plays a role in the assembly of snRNP core particles. May play a role in cytokine-activated transduction pathways. Negatively regulates cyclin E1 promoter activity and cellular proliferation. May regulate the SUPT5H transcriptional elongation properties. May be part of a pathway that is connected to a chloride current, possibly through cytoskeletal rearrangement. Methylates histone H2A and H4 'Arg-3' during germ cell development. Methylates histone H3 'Arg-8', which may repress transcription. Methylates the Piwi proteins (PIWIL1, PIWIL2 and PIWIL4), methylation of Piwi proteins being required for the interaction with Tudor domain-containing proteins and subsequent localization to the meiotic nuage. Methylates RPS10.

Function:
Arginine methyltransferase that can both catalyze the formation of omega-N monomethylarginine (MMA) and symmetrical dimethylarginine (sDMA), with a preference for the formation of MMA. Specifically mediates the symmetrical dimethylation of arginine residues in the small nuclear ribonucleoproteins Sm D1 (SNRPD1) and Sm D3 (SNRPD3); such methylation being required for the assembly and biogenesis of snRNP core particles. Methylates SUPT5H. Mono- and dimethylates arginine residues of myelin basic protein (MBP) in vitro. Plays a role in the assembly of snRNP core particles. May play a role in cytokine-activated transduction pathways. Negatively regulates cyclin E1 promoter activity and cellular proliferation. May regulate the SUPT5H transcriptional elongation properties. May be part of a pathway that is connected to a chloride current, possibly through cytoskeletal rearrangement. Methylates histone H2A and H4 'Arg-3' during germ cell development. Methylates histone H3 'Arg-8', which may repress transcription. Methylates the Piwi proteins (PIWIL1, PIWIL2 and PIWIL4), methylation of Piwi proteins being required for the interaction with Tudor domain-containing proteins and subsequent localization to the meiotic nuage. Methylates RPS10. Attenuates EGF signaling through the MAPK1/MAPK3 pathway acting at 2 levels. First, monomethylates EGFR; this enhances EGFR 'Tyr-1197' phosphorylation and PTPN6 recruitment, eventually leading to reduced SOS1 phosphorylation. Second, methylates RAF1 and probably BRAF, hence destabilizing these 2 signaling proteins and reducing their catalytic activity. Required for induction of E-selectin and VCAM-1, on the endothelial cells surface at sites of inflammation. Methylates HOXA9.

Subunit:
Forms, at least, homodimers and homotetramers. Interacts with PRDM1. Component of the methylosome, a 20S complex containing at least pICLn, PRMT1/SKB1 and MEP50. Component of a high molecular weight E2F-pocket protein complex, CERC (cyclin E1 repressor complex). Also interacts with Sm proteins, JAK2, SSTR1 and SUPT5H. Associates with SWI/SNF remodeling complexes containing SMARCA2 and SMARCA4. Interacts with LSM11, PRMT7 and SNRPD3. Interacts with COPR5/C17orf79; promoting its recruitment on histone H4. Interacts with RPS10. Interacts with EGFR; methylates EGFR and stimulates EGFR-mediated ERK activation. Interacts with BRAF and with active RAF1. Interacts with HOXA9.

Subcellular Location:
Cytoplasm. Nucleus.

Tissue Specificity:
Ubiquitous.

Post-translational modifications:
Disulfide bonds and non-covalent association mediate homooligomers formation.

Similarity:
Belongs to the protein arginine N-methyltransferase family.

Database links:

Entrez Gene: 10419 Human

Entrez Gene: 27374 Mouse

Entrez Gene: 364382 Rat

Omim: 604045 Human

SwissProt: O14744 Human

SwissProt: Q8CIG8 Mouse

Unigene: 367854 Human

Unigene: 196585 Mouse

Unigene: 101808 Rat



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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