phospho-Smad3 (Ser204)抗体特异性结合抗原：抗体本身不能直接溶解或杀伤带有特异抗原的靶细胞，通常需要补体或吞噬细胞等共同发挥效应以**病原微生物或导致病理损伤。然而，抗体可通过与病毒或**的特异性结合，直接发挥中和病毒的作用。
产品编号xy- 5235R
英文名称phospho-Smad3 (Ser204)
中文名称磷酸化细胞信号转导分子SMAD3抗体
别 名Smad3 (phospho S204); p-Smad3 (phospho S204); SMAD3(phospho S204); SMAD3(phospho Ser204); p-Smad3 (Ser204); 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.
说 明 书100ul
产品类型磷酸化抗体
研究领域肿瘤 细胞生物 **学 信号转导 干细胞 细胞凋亡 转录调节因子
抗体来源Rabbit
克隆类型Polyclonal
phospho-Smad3 (Ser204)抗体交叉反应 Human, Mouse, Rat, Pig, Cow, Horse, Rabbit, Sheep,
产品应用WB=1:500-2000 ELISA=1:500-1000 IHC-P=1:400-800 IHC-F=1:400-800 Flow-Cyt=1μg/Test ICC=1:100-500 IF=1:100-500 （石蜡切片需做抗原修复）
not yet tested in other applications.
optimal dilutions/concentrations should be determined by the end user.
分 子 量47kDa
细胞定位细胞核 细胞浆
性 状Lyophilized or Liquid
浓 度1mg/1ml
免 疫 原KLH conjugated Synthesised phosphopeptide derived from human Smad3 around the phosphorylation site of Ser204 [AG(p-S)PN]:AG(p-S)PN
亚 型IgG
纯化方法affinity purified by Protein A
储 存 液0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol.
phospho-Smad3 (Ser204)抗体保存条件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.
PubMedPubMed
产品介绍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.
SWISS:
P84022
Gene ID:
4088
phospho-Smad3 (Ser204)抗体（antibody,
Ab）是由效应B细胞（效应**B细胞）分泌，机体用于抵御外来物质，如病毒，**等抗原，结构呈“Y”字型的球状蛋白质，仅仅存在于脊椎动物的血液和B**细胞膜表面。凡是能够跟抗体结合的物质，均被称作抗原，因此对于抗抗体（能够结合抗体的抗体）来说，抗体本身也是一种抗原物质。
phospho-Smad3 (Ser204)抗体普通抗体重链和轻链的结构
重链结构：普通的**球蛋白具有2条重链（H链），分子量约为50kD,有μ、δ、γ、ε和α五种重链亚型，对应的**球蛋白名称分别为IgM、IgG、IgA、IgD和IgE。
轻链结构： 普通**球蛋白具有2条轻链（L链），分子质量约25kDa，有κ链和λ链两种亚型，这两种轻链决定了Ig的亚型类别（IgG1，IgG2，IgG3，IgG4）。一个天然的Ig分子两条轻链总是相同的，但在同一个体内可存在分别带有κ或λ链的抗体分子。不同种属生物体内两型轻链的比例不同，正常人血清**球蛋白κ链：λ链约为2：1，而在小鼠的比例为20：1。
2.2抗体Fab段和Fc段
IgG经木瓜蛋白酶酶切后裂解为2个完全相同的Fab段和1个Fc段,每个Fab段都为单价,可与抗原结合但不会再发生凝集反应；经胃蛋白酶酶切后裂解为1个完整F(ab)2片段和碎片化的Fc片段,F(ab’)2片段为双价,可同时结合两个抗原表位。Fab段为抗原结合片段（fragment of antigen binding，Fab），相当于抗体分子的两个臂，由一个完整的轻链和重链的VH和CH1结构域组成。Fc段为可结晶段（fragment crystallizable，Fc）相当于Ig的CH2和CH3结构域，是Ig与效应分子或者细胞相互作用的部位。Fab段包含完整的可变区，以及恒定区的CH1区域。Fc段仅指Ig恒定区CH2和CH3的区域，相当于Y字结构下面那一部分。
合格 IRAK1BP1 白细胞介素1受体相关激酶1结合蛋白1抗体
合格 IRF2BP2 干扰素调节因子2结合蛋白2抗体
合格 IRF5 干扰素调节因子5抗体
合格 TREX2 TREX2蛋白抗体
合格 phospho-TRF1 (Ser219) 磷酸化端粒体复制结合因子1抗体
合格 TRF4-2 拓扑异构酶相关功能蛋白4-2抗体
合格 TRH Receptor 促甲状腺**释放**受体抗体
合格 TRIM29 (acetyl K116) 乙酰化TRIM29蛋白抗体
合格 TRIM38 TRIM38蛋白抗体
合格 TRIM42 TRIM42蛋白抗体
合格 TRIM43B TRIM43B蛋白抗体
合格 TRIM45 TRIM45蛋白抗体
合格 TRIM49 TRIM49蛋白抗体
合格 TRIM50C TRIM50C蛋白抗体
合格 KLB KLB蛋白抗体
合格 KLC2 驱动蛋白轻链2抗体
合格 KLC4 驱动蛋白轻链4抗体
合格 合格 KLHDC1 KLHDC1蛋白抗体
合格 KLHDC10 KLHDC10蛋白抗体
合格 KLHDC2 肝癌相关抗原33抗体
合格 KLHDC4 KLHDC4蛋白抗体
合格 合格 KLHDC7B KLHDC7B蛋白抗体
合格 KLHDC8B KLHDC8B蛋白抗体