癌症的基本特征包括细胞增殖、血管生成、迁移、凋亡逃避机制和细胞永生等。找到癌症发生过程中这些通路的关键标记物和对应的抗体用于检测至关重要。
为您推荐一个泛素化位点预测神器——泛素化分析工具，可以为您的蛋白的泛素化位点作出预测和评分。
细胞自噬受体图形绘图工具为你的蛋白的细胞受体结合位点作出预测和评分，识别结合到自噬通路中的蛋白是非常重要的，便于让我们理解自噬在正常生理、病理过程中的作用，如发育、细胞分化、神经退化性疾病、压力条件下、感染和癌症。
Phospho-SMAD3(S208) Antibody
Affinity Purified Rabbit Polyclonal Antibody (Pab)
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- 文献引用 : 1
- 实验流程
- 背景知识
Application 
| IF, DB, E |
|---|---|
| Primary Accession | P84022 |
| Other Accession | P84025, P84024, Q8BUN5, P84023 |
| Reactivity | Human |
| Predicted | Chicken, Mouse, Pig, Rat |
| Host | Rabbit |
| Clonality | Polyclonal |
| Isotype | Rabbit IgG |
| Calculated MW | 48081 Da |
| Gene ID | 4088 |
|---|---|
| Other Names | Mothers against decapentaplegic homolog 3, MAD homolog 3, Mad3, Mothers against DPP homolog 3, hMAD-3, JV15-2, SMAD family member 3, SMAD 3, Smad3, hSMAD3, SMAD3, MADH3 |
| Target/Specificity | This SMAD3 Antibody is generated from rabbits immunized with a KLH conjugated synthetic phosphopeptide corresponding to amino acid residues surrounding S208 of human SMAD3. |
| Dilution | IF~~1:10~50 DB~~1:500 |
| Format | Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein A column, followed by peptide affinity purification. |
| Storage | Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles. |
| Precautions | Phospho-SMAD3(S208) Antibody is for research use only and not for use in diagnostic or therapeutic procedures. |
| Name | SMAD3 |
|---|---|
| Synonyms | MADH3 |
| 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. Positively regulates PDPK1 kinase activity by stimulating its dissociation from the 14-3-3 protein YWHAQ which acts as a negative regulator. |
| Cellular 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 (PubMed:15799969, PubMed:21145499). Through the action of the phosphatase PPM1A, released from the SMAD2/SMAD4 complex, and exported out of the nucleus by interaction with RANBP1 (PubMed:16751101, PubMed:19289081). Co-localizes with LEMD3 at the nucleus inner membrane (PubMed:15601644). MAPK-mediated phosphorylation appears to have no effect on nuclear import (PubMed:19218245). PDPK1 prevents its nuclear translocation in response to TGF-beta (PubMed:17327236). Localized mainly to the nucleus in the early stages of embryo development with expression becoming evident in the cytoplasm of the inner cell mass at the blastocyst stage (By similarity) {ECO:0000250|UniProtKB:Q8BUN5, ECO:0000269|PubMed:15601644, ECO:0000269|PubMed:15799969, ECO:0000269|PubMed:16751101, ECO:0000269|PubMed:17327236, ECO:0000269|PubMed:19218245, ECO:0000269|PubMed:19289081, ECO:0000269|PubMed:21145499} |
Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
SMAD3, a receptor regulated SMAD (R-SMAD) is a transcriptional modulator activated by TGF-beta (transforming growth factor) and activin type 1 receptor kinase. SMAD3 is estimated to account for at least 80% of all TGF-beta-mediated response. Activated type I receptor phosphorylates receptor-activated SMADS (RSMADS) at their c-terminal two extreme serines in the SSXS motif. The phosphorylated R-SMAD translocate into nucleus, where they regulate transcription of target genes. SMAD3 signal transduction appears to be important in the rgulation of muscle-specific genes. Loss of SMAD3 is a feature of pediatric T-cell lymphoblastic leukemia, while upregulation of SMAD3 may be responsible for TGFB hyperresponsiveness observed in scleroderma.
REFERENCES
References for protein:
1.Imoto, S., et al., FEBS Lett. 579(13):2853-2862 (2005).
2.Dubrovska, A., et al., Oncogene 24(14):2289-2297 (2005).
3.Furumatsu, T., et al., J. Biol. Chem. 280(9):8343-8350 (2005).
4.Kobayashi, T., et al., Biochem. Biophys. Res. Commun. 327(2):393-398 (2005).
5.Kamaraju, A.K., et al., J. Biol. Chem. 280(2):1024-1036 (2005).
References for HeLa cell line:
1. Scherer WF, Syverton JT, Gey GO (May 1953). "Studies on the propagation in vitro of poliomyelitis viruses. IV. Viral multiplication in a stable strain of human malignant epithelial cells (strain HeLa) derived from an epidermoid carcinoma of the cervix". J. Exp. Med. 97 (5): 695–710. [PubMed:13052828].
2. Macville M, Schröck E, Padilla-Nash H, Keck C, Ghadimi BM, Zimonjic D, Popescu N, Ried T (January 1999). "Comprehensive and definitive molecular cytogenetic characterization of HeLa cells by spectral karyotyping". Cancer Res. 59 (1): 141–50. [PubMed: 9892199].
3. Rahbari R, Sheahan T, Modes V, Collier P, Macfarlane C, Badge RM (April 2009). "A novel L1 retrotransposon marker for HeLa cell line identification". BioTechniques 46 (4): 277–84. [PubMed: 19450234].
4. Capes-Davis A, Theodosopoulos G, Atkin I, Drexler HG, Kohara A, MacLeod RA, Masters JR, Nakamura Y, Reid YA, Reddel RR, Freshney RI (July 2010). "Check your cultures! A list of cross-contaminated or misidentified cell lines". Int. J. Cancer 127 (1): 1–8. [PubMed:20143388].
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