亚洲中文字幕特级毛片-亚洲制服丝袜中文字幕-亚洲制服丝袜在线观看-亚洲制服欧美自拍另类-免费一级黄色-免费一级国产生活片

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  聯系我們
口国产成人高清在线播放,色老头老太xxxxbbbb,伊人久久大香线蕉精品
首頁 > 產品中心 > 標記一抗 > 產品信息
Rabbit Anti-phospho-Smad3 (Ser423)/Gold Conjugated antibody (bs-2225R-Gold)
訂購熱線:400-901-9800
訂購郵箱:sales@www.chomd.com.cn
訂購QQ:  400-901-9800
技術支持:techsupport@www.chomd.com.cn
說 明 書: 100ul(10nm  15nm  35nm
100ul/2980.00元
大包裝/詢價
產品編號 bs-2225R-Gold
英文名稱1 Rabbit Anti-phospho-Smad3 (Ser423)/Gold Conjugated antibody
中文名稱 膠體金標記的磷酸化細胞信號轉導分子SMAD3抗體
別    名 Smad3 (phospho Ser423); Smad3 (phospho S423); p-Smad3 (Ser423); 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.   
規格價格 100ul/2980元 購買        大包裝/詢價
說 明 書 100ul(10nm  15nm  35nm
產品類型 磷酸化抗體 
研究領域 腫瘤  細胞生物  信號轉導  干細胞  細胞凋亡  生長因子和激素  轉錄調節因子  
抗體來源 Rabbit
克隆類型 Polyclonal
交叉反應 Human,  (predicted: Mouse, Rat, Pig, )
產品應用 IEM=1:20-200 ICA=1:20-200 ChIP=1:20-200 
not yet tested in other applications.
optimal dilutions/concentrations should be determined by the end user.
性    狀 Lyophilized or Liquid
濃    度 0.4mg/ml
免 疫 原 KLH conjugated Synthesised phosphopeptide derived from human Smad3 around the phosphorylation site of Ser423
亞    型 IgG
純化方法 affinity purified by Protein A
儲 存 液 0.02M TBS(pH8.2) with 1% BSA, 0.03% Proclin300.
保存條件 Store at 2-8 oC for 3-6 months. Avoid repeated freeze/thaw cycles.
產品介紹 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.www.chomd.com.cn 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         京公網安備110107000727號
主站蜘蛛池模板: 亚洲AV无码专区在线播放中文qu| 小森林电影高清完整版在线观看| 免费一区二区无码视频在线播放网站| 中文字幕爆乳巨爆乳系列无码拳交片 | 久久精品一区二区三区不卡68少妇 | 久久久久久午夜成人影院黑人专门区 | 婷婷综合狠狠热| 精品国产一区二区三区香蕉笑了| JULIA中文字幕在线看| 亚洲日本一本palipali2轻量| 免费观看黄色的网站,一区二区三区级二级三级 | 一区 二区 三区 中文字幕视频| 无码中文字幕日韩专区下载_蜜臀av | 色综合久久久无码中文字幕麻豆 | 中文字幕av无码不卡免费、亚洲成av人片 | 麻豆短视频在线观看成人| 国产护士在线观看视频播放| 亚洲中文无码免费论坛爱情岛| 久久人做人爽一区二区三区2024 | 男女猛烈激情XX00免费视频美国 | 久久9精品区-无套内射无码漫画 | 中文字幕在线视频第一页观看 | 一本无码在线观看免费九九| 久久久久久亚洲中文字幕不卡| 3p黑人国产亚洲一区| 中文字幕久无码久久久久| 日韩超碰人人爽人人做人人添_ | 亚洲美女群交颜射吞精小说 | 亚洲精品专区在线观看污| 精品国产导航网址一区| 亚洲美女大胸诱惑视频在线观看 | 一级毛片视频播放一一| 精品国产污污免费网站东 | 国产亚洲精久久久久久无码的演员有哪些| 制服中文字幕一区二区三区牛牛影视视频姿原 | 91精品国产91久久综合下面有根棒棒糖| 午夜精品久久久久成人孕妇内射| 国产91嫩草精品| 日本黄网站动漫视频免费播放| 51国产黑色丝袜高跟鞋美女| 久久精品国产久精国产|亚洲日韩中文第一精品 |