吃奶呻吟打开双腿做受动态图 -亚洲色偷偷色噜噜狠狠99网-日韩精品极品视频在线观看免费-来一水AV@lysav

掃碼關注公眾號           掃碼咨詢技術支持           掃碼咨詢技術服務
  
客服熱線:400-901-9800  客服QQ:4009019800  技術答疑  技術支持  質量反饋  人才招聘  關于我們  聯(lián)系我們
潘金莲被武松高潮八次小说,国产亚洲精品久久久无码,扒开腿挺进湿润的花苞
首頁 > 產(chǎn)品中心 > 標記一抗 > 產(chǎn)品信息
Rabbit Anti-Smad3/BF647 Conjugated antibody (bsm-52224R-BF647)
訂購熱線:400-901-9800
訂購郵箱:sales@xucheq.com
訂購QQ:  400-901-9800
技術支持:techsupport@xucheq.com
說 明 書: 100ul  
100ul/2980.00元
大包裝/詢價
產(chǎn)品編號 bsm-52224R-BF647
英文名稱1 Rabbit Anti-Smad3/BF647 Conjugated antibody
中文名稱 BF647標記的兔抗細胞信號轉導分子SMAD3單克隆抗體
別    名 hMAD 3; hSMAD3; HSPC193; JV15 2; JV152; MAD (mothers against decapentaplegic Drosophila) homolog 3; MAD3; MADH 3; MADH3; Mothers against decapentaplegic homolog 3; Mothers against DPP homolog 3; SMA and MAD related protein 3; SMAD 3; SMAD; SMAD-3; SMAD3_HUMAN.  
規(guī)格價格 100ul/2980元 購買        大包裝/詢價
說 明 書 100ul  
研究領域 腫瘤  細胞生物  免疫學  信號轉導  干細胞  細胞凋亡  生長因子和激素  轉錄調節(jié)因子  
抗體來源 Rabbit
克隆類型 Monoclonal
克 隆 號 3D1
交叉反應 (predicted: Human, Mouse, Rat, )
產(chǎn)品應用 ICC=1:50-200 IF=1:50-200 
not yet tested in other applications.
optimal dilutions/concentrations should be determined by the end user.
分 子 量 47kDa
性    狀 Lyophilized or Liquid
濃    度 1mg/ml
免 疫 原 Recombinant human Smad3
亞    型 IgG
純化方法 affinity purified by Protein A
儲 存 液 Preservative: 15mM Sodium Azide, Constituents: 1% BSA, 0.01M PBS, pH 7.4.
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:
Smad3 is a 50 kDa member of a family of proteins that act as key mediators of TGF beta superfamily signaling in cell proliferation, differentiation and development. The Smad family is divided into three subclasses: receptor regulated Smads, activin/TGF beta receptor regulated (Smad2 and 3) or BMP receptor regulated (Smad 1, 5, and 8); the common partner, (Smad4) that functions via its interaction to the various Smads; and the inhibitory Smads, (Smad6 and 7). Activated Smad3 oligomerizes with Smad4 upon TGF beta stimulation and translocates as a complex into the nucleus, allowing its binding to DNA and transcription factors. Phosphorylation of the two TGF beta dependent serines 423 and 425 in the C terminus of Smad3 is critical for Smad3 transcriptional activity and TGF beta signaling.

Function:
Receptor-regulated SMAD (R-SMAD) that is an intracellular signal transducer and transcriptional modulator activated by TGF-beta (transforming growth factor) and activin type 1 receptor kinases. Binds the TRE element in the promoter region of many genes that are regulated by TGF-beta and, on formation of the SMAD3/SMAD4 complex, activates transcription. Also can form a SMAD3/SMAD4/JUN/FOS complex at the AP-1/SMAD site to regulate TGF-beta-mediated transcription. Has an inhibitory effect on wound healing probably by modulating both growth and migration of primary keratinocytes and by altering the TGF-mediated chemotaxis of monocytes. This effect on wound healing appears to be hormone-sensitive. Regulator of chondrogenesis and osteogenesis and inhibits early healing of bone fractures (By similarity). Positively regulates PDPK1 kinase activity by stimulating its dissociation from the 14-3-3 protein YWHAQ which acts as a negative regulator.

Subunit:
Monomer; in the absence of TGF-beta. Homooligomer; in the presence of TGF-beta. Heterotrimer; forms a heterotrimer in the presence of TGF-beta consisting of two molecules of C-terminally phosphorylated SMAD2 or SMAD3 and one of SMAD4 to form the transcriptionally active SMAD2/SMAD3-SMAD4 complex. Interacts with TGFBR1. Part of a complex consisting of AIP1, ACVR2A, ACVR1B and SMAD3. Interacts with AIP1, TGFB1I1, TTRAP, FOXL2, PML, PRDM16, HGS and WWP1. Interacts (via MH2 domain) with CITED2 (via C-terminus) (By similarity). Interacts with NEDD4L; the interaction requires TGF-beta stimulation (By similarity). Interacts (via the MH2 domain) with ZFYVE9. Interacts with HDAC1, VDR, TGIF and TGIF2, RUNX3, CREBBP, SKOR1, SKOR2, SNON, ATF2, SMURF2 and TGFB1I1. Interacts with DACH1; the interaction inhibits the TGF-beta signaling. Forms a complex with SMAD2 and TRIM33 upon addition of TGF-beta. Found in a complex with SMAD3, RAN and XPO4. Interacts in the complex directly with XPO4. Interacts (via the MH2 domain) with LEMD3; the interaction represses SMAD3 transcriptional activity through preventing the formation of the heteromeric complex with SMAD4 and translocation to the nucleus. Interacts with RBPMS. Interacts (via MH2 domain) with MECOM. Interacts with WWTR1 (via its coiled-coil domain). Interacts (via the linker region) with EP300 (C-terminal); the interaction promotes SMAD3 acetylation and is enhanced by TGF-beta phosphorylation in the C-terminal of SMAD3. This interaction can be blocked by competitive binding of adenovirus oncoprotein E1A to the same C-terminal site on EP300, which then results in partially inhibited SMAD3/SMAD4 transcriptional activity. Interacts with SKI; the interaction represses SMAD3 transcriptional activity. Component of the multimeric complex SMAD3/SMAD4/JUN/FOS which forms at the AP1 promoter site; required for syngernistic transcriptional activity in response to TGF-beta. Interacts (via an N-terminal domain) with JUN (via its basic DNA binding and leucine zipper domains); this interaction is essential for DNA binding and cooperative transcriptional activity in response to TGF-beta. Interacts with PPM1A; the interaction dephosphorylates SMAD3 in the C-terminal SXS motif leading to disruption of the SMAD2/3-SMAD4 complex, nuclear export and termination of TGF-beta signaling. Interacts (dephosphorylated form via the MH1 and MH2 domains) with RANBP3 (via its C-terminal R domain); the interaction results in the export of dephosphorylated SMAD3 out of the nucleus and termination of the TGF-beta signaling. Interacts with MEN1. Interacts with IL1F7. Interaction with CSNK1G2. Interacts with PDPK1 (via PH domain).

Subcellular Location:
Cytoplasm. Nucleus. Note=Cytoplasmic and nuclear in the absence of TGF-beta. On TGF-beta stimulation, migrates to the nucleus when complexed with SMAD4. Through the action of the phosphatase PPM1A, released from the SMAD2/SMAD4 complex, and exported out of the nucleus by interaction with RANBP1. Co-localizes with LEMD3 at the nucleus inner membrane. MAPK-mediated phosphorylation appears to have no effect on nuclear import. PDPK1 prevents its nuclear translocation in response to TGF-beta.

Post-translational modifications:
Phosphorylated on serine and threonine residues. Enhanced phosphorylation in the linker region on Thr-179, Ser-204 and Ser-208 on EGF AND TGF-beta treatment. Ser-208 is the main site of MAPK-mediated phosphorylation. CDK-mediated phosphorylation occurs in a cell-cycle dependent manner and inhibits both the transcriptional activity and antiproliferative functions of SMAD3. This phosphorylation is inhibited by flavopiridol. Maximum phosphorylation at the G(1)/S junction. Also phosphorylated on serine residues in the C-terminal SXS motif by TGFBR1 and ACVR1. TGFBR1-mediated phosphorylation at these C-terminal sites is required for interaction with SMAD4, nuclear location and transactivational activity, and appears to be a prerequisite for the TGF-beta mediated phosphorylation in the linker region. Dephosphorylated in the C-terminal SXS motif by PPM1A. This dephosphorylation disrupts the interaction with SMAD4, promotes nuclear export and terminates TGF-beta-mediated signaling. Phosphorylation at Ser-418 by CSNK1G2/CK1 promotes ligand-dependent ubiquitination and subsequent proteasome degradation, thus inhibiting SMAD3-mediated TGF-beta responses. Phosphorylated by PDPK1.
Acetylation in the nucleus by EP300 in the MH2 domain regulates positively its transcriptional activity and is enhanced by TGF-beta.
Ubiquitinated.

DISEASE:
Defects in SMAD3 may be a cause of colorectal cancer (CRC) [MIM:114500].
Defects in SMAD3 are the cause of Loeys-Dietz syndrome type 1C (LDS1C) [MIM:613795]. LDS1C is an aortic aneurysm syndrome with widespread systemic involvement. The disorder is characterized by the triad of arterial tortuosity and aneurysms, hypertelorism, and bifid uvula or cleft palate. Patients with LDS1C also manifest early-onset osteoarthritis. They lack craniosynostosis and mental retardation.

Similarity:
Belongs to the dwarfin/SMAD family.
Contains 1 MH1 (MAD homology 1) domain.
Contains 1 MH2 (MAD homology 2) domain.

Database links:

Entrez Gene: 4088 Human

Entrez Gene: 17127 Mouse

Entrez Gene: 25631 Rat

Omim: 603109 Human

SwissProt: P84022 Human

SwissProt: Q8BUN5 Mouse

SwissProt: P84025 Rat

Unigene: 727986 Human

Unigene: 7320 Mouse

Unigene: 10636 Rat



Important Note:
This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.
版權所有 2004-2026 www.xucheq.com 北京博奧森生物技術有限公司
通過國際質量管理體系ISO 9001:2015 GB/T 19001-2016    證書編號: 00124Q34771R2M/1100
通過國際醫(yī)療器械-質量管理體系ISO 13485:2016 GB/T 42061-2022    證書編號: CQC24QY10047R0M/1100
京ICP備05066980號-1         京公網(wǎng)安備110107000727號
最近2019中文字幕大全第二页| 日本无翼乌邪恶大全彩H| 国产裸拍裸体视频在线观看| 日本熟妇色XXXXX日本免费看, | 久久精品亚洲一区二区三区浴池 | 国产性生大片免费观看性| 国产美女视频黄A片免费观看软件| 欧美大荫蒂AV高潮| 97在线视频人妻无码| 精品人妻码一区二区三区| 人与禽性视频77777| 中文字幕丰满伦子无码| 中文字幕在线观看| 又大又紧又粉嫩18P少妇| 国产强被迫伦姧在线观看无码| 无套熟女AV呻吟在线观看| 亚婷婷洲AV久久蜜臀无码| 免费国产又色又爽又黄的网站| 老师说我考好了就随便我怎样| 一本色道久久88加勒比—综合| 精品久久久久久无码中文字幕一区 | 精品少妇无码AV无码专区| 无码精品人妻一区二区三区人妻斩| 欧美成人片一区二区三区| 丁香婷婷综合激情五月色| 亚洲中文字幕在线观看| 99热久久这里只精品国产WWW| 色一情一乱一乱一区99AV| 高潮影院| 大肉大捧一进一出好爽视频MBA| 久久久久亚洲AV无码专区| 大胸美女视频| 亚洲熟女乱综合一区二区| 色一情一区二| 玩弄白嫩少妇XXXXX性| 小12箩利洗澡无码视频网站| 国产乱人对白A片麻豆| 久久久久久久99精品免费观看 | 国产深夜男女无套内射 | 性欧美xxxxx乱极品少妇| 人妻精品久久久久中文字幕|