Phospho-Smad7 (Ser249) Antibody - #AF3827

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Product: Phospho-Smad7 (Ser249) Antibody
Catalog: AF3827
Description: Rabbit polyclonal antibody to Phospho-Smad7 (Ser249)
Application: IHC
Reactivity: Human, Mouse, Rat
Mol.Wt.: 46kD(Calculated).
Uniprot: O15105
RRID: AB_2847141

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 100ul $350 In stock
 200ul $450 In stock

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Related Downloads
MSDS
Data Sheet
COA
Protocols
WB Handbook
IHC Protocol
IF/ICC Protocol

Product Info

Source:
Rabbit
Application:
IHC 1:50-1:200
*The optimal dilutions should be determined by the end user.
*Tips:

WB: For western blot detection of denatured protein samples. IHC: For immunohistochemical detection of paraffin sections (IHC-p) or frozen sections (IHC-f) of tissue samples. IF/ICC: For immunofluorescence detection of cell samples. ELISA(peptide): For ELISA detection of antigenic peptide.

Reactivity:
Human,Mouse,Rat
Clonality:
Polyclonal
Specificity:
Phospho-Smad7 (Ser249) Antibody detects endogenous levels of Smad7 only when phosphorylated at Ser249.
RRID:
AB_2847141
Cite Format: Affinity Biosciences Cat# AF3827, RRID:AB_2847141.
Conjugate:
Unconjugated.
Purification:
The antibody is from purified rabbit serum by affinity purification via sequential chromatography on phospho-peptide and non-phospho-peptide affinity columns.
Storage:
Rabbit IgG in phosphate buffered saline , pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol. Store at -20 °C. Stable for 12 months from date of receipt.
Alias:

Fold/Unfold

CRCS3; FLJ16482; hSMAD 7; hSMAD7; MAD (mothers against decapentaplegic Drosophila) homolog 7; MAD; Mad homolog 7; MAD homolog 8; MAD mothers against decapentaplegic homolog 7; MADH 7; MADH 8; MADH6; MADH7; MADH8; Mothers Against Decapentaplegic Drosophila Homolog of 6; Mothers Against Decapentaplegic Drosophila Homolog of 7; Mothers against decapentaplegic homolog 7; Mothers against decapentaplegic homolog 8; Mothers against DPP homolog 7; Mothers against DPP homolog 8; SMA- AND MAD-RELATED PROTEIN 7; SMAD 7; SMAD; SMAD family member 7; SMAD, mothers against DPP homolog 7 (Drosophila); SMAD, mothers against DPP homolog 7; SMAD6; Smad7; SMAD7_HUMAN;

Immunogens

Immunogen:

A synthesized peptide derived from human Smad7 around the phosphorylation site of Ser249.

Uniprot:

O15105(SMAD7_HUMAN) >>Visit HPA database.

Gene(ID):
SMAD7(4092)
Expression:
O15105 SMAD7_HUMAN:

Ubiquitous with higher expression in the lung and vascular endothelium.

Sequence:
MFRTKRSALVRRLWRSRAPGGEDEEEGAGGGGGGGELRGEGATDSRAHGAGGGGPGRAGCCLGKAVRGAKGHHHPHPPAAGAGAAGGAEADLKALTHSVLKKLKERQLELLLQAVESRGGTRTACLLLPGRLDCRLGPGAPAGAQPAQPPSSYSLPLLLCKVFRWPDLRHSSEVKRLCCCESYGKINPELVCCNPHHLSRLCELESPPPPYSRYPMDFLKPTADCPDAVPSSAETGGTNYLAPGGLSDSQLLLEPGDRSHWCVVAYWEEKTRVGRLYCVQEPSLDIFYDLPQGNGFCLGQLNSDNKSQLVQKVRSKIGCGIQLTREVDGVWVYNRSSYPIFIKSATLDNPDSRTLLVHKVFPGFSIKAFDYEKAYSLQRPNDHEFMQQPWTGFTVQISFVKGWGQCYTRQFISSCPCWLEVIFNSR

PTMs - O15105 As Substrate

Site PTM Type Enzyme
K64 Acetylation
K64 Ubiquitination
K70 Acetylation
K70 Methylation
K70 Ubiquitination
T96 Phosphorylation Q14680 (MELK)
K101 Ubiquitination
S117 Phosphorylation
T121 Phosphorylation
S249 Phosphorylation
T354 Phosphorylation

Research Backgrounds

Function:

Antagonist of signaling by TGF-beta (transforming growth factor) type 1 receptor superfamily members; has been shown to inhibit TGF-beta (Transforming growth factor) and activin signaling by associating with their receptors thus preventing SMAD2 access. Functions as an adapter to recruit SMURF2 to the TGF-beta receptor complex. Also acts by recruiting the PPP1R15A-PP1 complex to TGFBR1, which promotes its dephosphorylation. Positively regulates PDPK1 kinase activity by stimulating its dissociation from the 14-3-3 protein YWHAQ which acts as a negative regulator.

PTMs:

Phosphorylation on Ser-249 does not affect its stability, nuclear localization or inhibitory function in TGFB signaling; however it affects its ability to regulate transcription (By similarity). Phosphorylated by PDPK1.

Ubiquitinated by WWP1 (By similarity). Polyubiquitinated by RNF111, which is enhanced by AXIN1 and promotes proteasomal degradation. In response to TGF-beta, ubiquitinated by SMURF1; which promotes its degradation.

Acetylation prevents ubiquitination and degradation mediated by SMURF1.

Subcellular Location:

Nucleus. Cytoplasm.
Note: Interaction with NEDD4L or RNF111 induces translocation from the nucleus to the cytoplasm (PubMed:16601693). TGF-beta stimulates its translocation from the nucleus to the cytoplasm. PDPK1 inhibits its translocation from the nucleus to the cytoplasm in response to TGF-beta (PubMed:17327236).

Extracellular region or secreted Cytosol Plasma membrane Cytoskeleton Lysosome Endosome Peroxisome ER Golgi apparatus Nucleus Mitochondrion Manual annotation Automatic computational assertionSubcellular location
Tissue Specificity:

Ubiquitous with higher expression in the lung and vascular endothelium.

Subunit Structure:

Interacts with WWP1 (By similarity). Interacts with COPS5. Interacts with NEDD4L. Interacts with STAMBP. Interacts with RNF111, AXIN1 and AXIN2. Interacts with PPP1R15A. Interacts (via MH2 domain) with EP300. Interacts with ACVR1B, SMURF1, SMURF2 and TGFBR1; SMAD7 recruits SMURF1 and SMURF2 to the TGF-beta receptor and regulates its degradation. Interacts with PDPK1 (via PH domain).

Family&Domains:

Belongs to the dwarfin/SMAD family.

Research Fields

· Environmental Information Processing > Signal transduction > TGF-beta signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > Hippo signaling pathway.   (View pathway)

References

1). Molecular mechanism of Gan-song Yin inhibiting the proliferation of renal tubular epithelial cells by regulating miR-21-5p in adipocyte exosomes. Journal of ethnopharmacology, 2024 (PubMed: 38043753) [IF=5.4]

Application: WB    Species: Mouse    Sample: TCMK-1 cells

Fig. 4. Mechanism of GSY on TCMK-1. A. Viability of TCMK-1 cells treated with different concentrations of GSY. B. TCMK-1 cell viability in each experimental group. C. Changes in TCMK-1 cell cycle level after GSY intervention. D. Changes in apoptosis level of TCMK-1 cells after GSY intervention. E. Expression of TGF-β1, SMAD2, SMAD3, SMAD7, p-SMAD2, p-SMAD3 and p-SMAD7 proteins in TCMK-1 cells after GSY intervention. F. Gene expression levels of TGF-β1, SMAD2, SMAD3 and SMAD7 in TCMK-1 cells after GSY intervention. *p < 0.05; **p < 0.01; ***p < 0.001. NC: Negative control; MOD: Model (60 mmol/L glucose). All experiments were repeated three times.
2). Mesenchymal stem cells ameliorate silica‐induced pulmonary fibrosis by inhibition of inflammation and epithelial‐mesenchymal transition. JOURNAL OF CELLULAR AND MOLECULAR MEDICINE, 2021 (PubMed: 34076355) [IF=5.3]

Application: WB    Species: Rat    Sample: lung tissues

FIGURE 5 BMSCs blocked the activation of TGF‐β/Smad pathway. (A) The mRNA expression of TGF‐β1 in lung tissue. n = 3 rats per group. (B) The protein expression levels of TGF‐β1 in lung tissues detected by ELISA. n = 7 rats per group. (C) The protein expression levels of TGF‐β1 in BALF detected by ELISA. n = 3 rats per group. (D) Western blot results of TGF‐β1, Smad2, p‐Smad2, Smad3, p‐Smad3 and Smad7 protein expression levels. n = 3 rats per group. (E‐H) The quantitative protein expression of TGF‐β1, p‐Smad2, p‐Smad3 and Smad7 in lung tissues. mRNA expression values were normalized to GAPDH. Data were presented as mean ± SD. * P <.05, ** P <.01
3). Cyclin-dependent kinase subunit2 (CKS2) promotes malignant phenotypes and epithelial-mesenchymal transition-like process in glioma by activating TGFβ/SMAD signaling. Cancer Medicine, 2023 (PubMed: 36284444) [IF=4.0]

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