Smad3 [p Ser423, p Ser425] Antibody - BSA Free

Novus Biologicals | Catalog # NBP1-77836

Novus Biologicals
100% Guarantee

Key Product Details

Validated by

Biological Validation

Species Reactivity

Validated:

Human, Mouse

Cited:

Human, Mouse

Applications

Validated:

Immunohistochemistry, Immunohistochemistry-Paraffin, Western Blot, ELISA, Flow Cytometry, Immunocytochemistry/ Immunofluorescence, Single Cell Western

Cited:

Western Blot, Immunocytochemistry/ Immunofluorescence, IF/IHC

Label

Unconjugated

Antibody Source

Polyclonal Rabbit IgG

Format

BSA Free
View all Smad3 Primary Antibodies »

Product Specifications

Immunogen

Smad3 [p Ser423, p Ser425] Antibody was prepared from whole rabbit serum produced by repeated immunizations with a dual phosphorylated synthetic peptide corresponding to a c-terminal region with Serine 423 and Serine 425 of human Smad3 protein. (Uniprot: P84022)

Reactivity Notes

A BLAST analysis was used to suggest cross reactivity with Smad3 from Xenopus laevis, Xenopus tropicalis, zebrafish, swine, bovine and chicken based on 100% sequence homology with the immunogen. Reactivity against homologues from other sources is not known

Modification

p Ser423, p Ser425

Specificity

This affinity-purified antibody is directed against the phosphorylated form of human Smad3 protein at the pS423 and pS425 residues. The resultant affinity purified antibody was then cross adsorbed against the non-phosphorylated form of the immunizing peptide. Reactivity occurs against human Smad3 pS423 and pS425 protein and the antibody is specific for the phosphorylated form of the protein. Reactivity with non-phosphorylated human Smad3 is minimal by ELISA and western blot. Expect reactivity against phosphorylated Smad1 and Smad5. Negligible reactivity is seen against other phosphorylated Smad family members. A BLAST analysis was used to suggest cross reactivity with Smad3 from human, Xenopus laevis, Xenopus tropicalis, zebrafish, rat, mouse, swine, bovine and chicken based on 100% sequence homology with the immunogen. Reactivity against homologues from other sources is not known.

Clonality

Polyclonal

Host

Rabbit

Isotype

IgG

Description

This affinity-purified antibody is directed against the phosphorylated form of human Smad3 protein at the [p Ser423] and [p Ser425] residues. The product was affinity purified from monospecific antiserum by immunoaffinity purification. Antiserum was first purified against the phosphorylated form of the immunizing peptide. The resultant affinity purified antibody was then cross adsorbed against the non-phosphorylated form of the immunizing peptide

Store vial at -20C prior to opening. Aliquot contents and freeze at -20C or below for extended storage. Avoid cycles of freezing and thawing. Centrifuge product if not completely clear after standing at room temperature. This product is stable for several weeks at 4C as an undiluted liquid. Dilute only prior to immediate use.

Scientific Data Images for Smad3 [p Ser423, p Ser425] Antibody - BSA Free

Western Blot: Smad3 [p Ser423, p Ser425] Antibody [NBP1-77836]

Western Blot: Smad3 [p Ser423, p Ser425] Antibody [NBP1-77836]

Western Blot: Smad3 [p Ser423, p Ser425] Antibody [NBP1-77836] - Shows detection of endogenous Smad3 in stimulated cell lysates. Lysates were prepared from control cells (- lanes), or cells stimulated with 2 ng/ml TGF (+lanes) for 1 hour. This reagent recognizes phosphorylated Smad3 and has negligible reactivity against non-phosphorylated Smad3 protein. Personal Communication. YIgG Zhang, NIH, CCR, Bethesda, MD.
Immunocytochemistry/ Immunofluorescence: Smad3 [p Ser423, p Ser425] Antibody [NBP1-77836]

Immunocytochemistry/ Immunofluorescence: Smad3 [p Ser423, p Ser425] Antibody [NBP1-77836]

Smad3-[p-Ser423--p-Ser425]-Antibody-Immunocytochemistry-Immunofluorescence-NBP1-77836-img0007.jpg
Immunohistochemistry: Smad3 [p Ser423, p Ser425] Antibody [NBP1-77836]

Immunohistochemistry: Smad3 [p Ser423, p Ser425] Antibody [NBP1-77836]

Immunohistochemistry: Smad3 [p Ser423, p Ser425] Antibody [NBP1-77836] - Used at 2.5 ug/ml to detect signal in a variety of tissues including multi-human, multi-brain and multi-cancer slides. This image shows strong nuclear staining in the majority of epidermal keratinocytes at 40X. Tissue was formalin-fixed and paraffin embedded. The image shows localization of the antibody as the precipitated red signal, with a hematoxylin purple nuclear counterstain. Personal Communication, Tina Roush, LifeSpanBiosciences, Seattle, WA.
Smad3 [p Ser423, p Ser425] Antibody

Smad3 [p Ser423, p Ser425] Antibody

Western Blot of Rabbit anti-SMAD3 pS423 pS425 antibody. Marker: Opal Pre-stained ladder
Smad3 [p Ser423, p Ser425] Antibody - BSA Free

Western Blot: Smad3 [p Ser423, p Ser425] Antibody - BSA Free [NBP1-77836] -

Mechanistic studies (I): Roflumilast prevents TGF beta 1-induced phospho-SMAD3 by the increase of PPM1A, the inhibition of reactive oxygen species (ROS) and phospho-ERK1/2-Protein Kinase A axis. Human keratinocytes were incubated for 30 min with vehicle or roflumilast (Rof, 100 nM) (A-F), the SMAD3 inhibitor (SIS3, 10uM) (A), the anti-oxidant N-acetyl-L-cysteine (NAC, 1 mM) (B, E), the PPM1A inhibitor sanguinarine (San, 3 uM) (D), the proteasome inhibitor MG132 (MG132, 5 uM) (E), the PKA inhibitor (KT5720, 2uM) (C), the ERK1/2 inhibitor (PD98059, 10uM) (F) or combinations as indicated. Next, keratinocytes were stimulated with TGF beta 1 (10 ng/ml) for 30 min and p-SMAD3 and PPM1A proteins were analysed by Western blotting. Data are shown from densitometry as the ratio of target protein compared to beta -actin of three independent experiments per condition. Results of the densitometry are presented as scatter dot blot with median and interquartile range values. P-values are based on Kruskal-Wallis test followed by the Dunn’s post-hoc test Image collected and cropped by CiteAb from the following open publication (https://pubmed.ncbi.nlm.nih.gov/39223490), licensed under a CC-BY license. Not internally tested by Novus Biologicals.
Smad3 [p Ser423, p Ser425] Antibody - BSA Free

Western Blot: Smad3 [p Ser423, p Ser425] Antibody - BSA Free [NBP1-77836] -

Activin A facilitates TGF beta 1-induced type II receptor expression without altering TGF beta 1 receptor sensitivity in MC. a TGF beta 1 for 30 min increased TRII expression and Smad3 activation in whole cell lysate, and both were prevented by 24 h pretreatment with follistatin (n = 6). b There was no change in TRII transcript after 24 h of follistatin with or without TGF beta 1 for 30 min. c Pretreatment with an actA neutralizing antibody for 24 h inhibited acute (30 min) TGF beta 1-induced Smad3 activation and TRII upregulation (n = 6–7). These were similarly inhibited by downregulation of the actA type I receptor ALK4 with siRNA (d) (n = 3). e Pretreatment with actA (20 ng/ml) for 24 h did not affect acute TGF beta 1-induced Smad3 activation (n = 6). *, **, ****P < 0.05, 0.01, 0.0001; one-way ANOVA with Tukey’s multiple comparisons post hoc test Image collected and cropped by CiteAb from the following open publication (https://pubmed.ncbi.nlm.nih.gov/36717814), licensed under a CC-BY license. Not internally tested by Novus Biologicals.
Smad3 [p Ser423, p Ser425] Antibody - BSA Free

Western Blot: Smad3 [p Ser423, p Ser425] Antibody - BSA Free [NBP1-77836] -

Mechanistic studies (I): Roflumilast prevents TGF beta 1-induced phospho-SMAD3 by the increase of PPM1A, the inhibition of reactive oxygen species (ROS) and phospho-ERK1/2-Protein Kinase A axis. Human keratinocytes were incubated for 30 min with vehicle or roflumilast (Rof, 100 nM) (A-F), the SMAD3 inhibitor (SIS3, 10uM) (A), the anti-oxidant N-acetyl-L-cysteine (NAC, 1 mM) (B, E), the PPM1A inhibitor sanguinarine (San, 3 uM) (D), the proteasome inhibitor MG132 (MG132, 5 uM) (E), the PKA inhibitor (KT5720, 2uM) (C), the ERK1/2 inhibitor (PD98059, 10uM) (F) or combinations as indicated. Next, keratinocytes were stimulated with TGF beta 1 (10 ng/ml) for 30 min and p-SMAD3 and PPM1A proteins were analysed by Western blotting. Data are shown from densitometry as the ratio of target protein compared to beta -actin of three independent experiments per condition. Results of the densitometry are presented as scatter dot blot with median and interquartile range values. P-values are based on Kruskal-Wallis test followed by the Dunn’s post-hoc test Image collected and cropped by CiteAb from the following open publication (https://pubmed.ncbi.nlm.nih.gov/39223490), licensed under a CC-BY license. Not internally tested by Novus Biologicals.
Smad3 [p Ser423, p Ser425] Antibody - BSA Free

Western Blot: Smad3 [p Ser423, p Ser425] Antibody - BSA Free [NBP1-77836] -

Mechanistic studies (I): Roflumilast prevents TGF beta 1-induced phospho-SMAD3 by the increase of PPM1A, the inhibition of reactive oxygen species (ROS) and phospho-ERK1/2-Protein Kinase A axis. Human keratinocytes were incubated for 30 min with vehicle or roflumilast (Rof, 100 nM) (A-F), the SMAD3 inhibitor (SIS3, 10uM) (A), the anti-oxidant N-acetyl-L-cysteine (NAC, 1 mM) (B, E), the PPM1A inhibitor sanguinarine (San, 3 uM) (D), the proteasome inhibitor MG132 (MG132, 5 uM) (E), the PKA inhibitor (KT5720, 2uM) (C), the ERK1/2 inhibitor (PD98059, 10uM) (F) or combinations as indicated. Next, keratinocytes were stimulated with TGF beta 1 (10 ng/ml) for 30 min and p-SMAD3 and PPM1A proteins were analysed by Western blotting. Data are shown from densitometry as the ratio of target protein compared to beta -actin of three independent experiments per condition. Results of the densitometry are presented as scatter dot blot with median and interquartile range values. P-values are based on Kruskal-Wallis test followed by the Dunn’s post-hoc test Image collected and cropped by CiteAb from the following open publication (https://pubmed.ncbi.nlm.nih.gov/39223490), licensed under a CC-BY license. Not internally tested by Novus Biologicals.
Smad3 [p Ser423, p Ser425] Antibody - BSA Free

Western Blot: Smad3 [p Ser423, p Ser425] Antibody - BSA Free [NBP1-77836] -

Activin A facilitates TGF beta 1-induced type II receptor expression without altering TGF beta 1 receptor sensitivity in MC. a TGF beta 1 for 30 min increased TRII expression and Smad3 activation in whole cell lysate, and both were prevented by 24 h pretreatment with follistatin (n = 6). b There was no change in TRII transcript after 24 h of follistatin with or without TGF beta 1 for 30 min. c Pretreatment with an actA neutralizing antibody for 24 h inhibited acute (30 min) TGF beta 1-induced Smad3 activation and TRII upregulation (n = 6–7). These were similarly inhibited by downregulation of the actA type I receptor ALK4 with siRNA (d) (n = 3). e Pretreatment with actA (20 ng/ml) for 24 h did not affect acute TGF beta 1-induced Smad3 activation (n = 6). *, **, ****P < 0.05, 0.01, 0.0001; one-way ANOVA with Tukey’s multiple comparisons post hoc test Image collected and cropped by CiteAb from the following open publication (https://pubmed.ncbi.nlm.nih.gov/36717814), licensed under a CC-BY license. Not internally tested by Novus Biologicals.
Smad3 [p Ser423, p Ser425] Antibody - BSA Free

Western Blot: Smad3 [p Ser423, p Ser425] Antibody - BSA Free [NBP1-77836] -

Specific activin A inhibition attenuates TGF beta 1-induced Smad3 activation and profibrotic responses in MC. a ELISA demonstrates that TGF beta 1 (24 h) increases actA and actB secretion (n = 3) to 19.5 ng/ml and 2.5 ng/ml, representing an 8.9- and 1.06-fold induction respectively. b TGF beta 1 increases actA in whole cell lysate by 1.8-fold (n = 3). c ActA (20 ng/ml) upregulates FN (n = 3–4), CTGF (n = 4) and alpha SMA (n = 6) at 48 h. d TGF beta 1 and actA both increase Smad3 transcriptional activity; no synergistic effect is seen (n = 6–12). e An actA neutralizing antibody attenuates TGF beta 1-induced FN (n = 5–6), alpha SMA (n = 5), CTGF (n = 5–6), and Smad3 activation (n = 10–12). f ActA neutralization decreases TGF beta 1-induced Smad3 transcriptional activity at 24 h (n = 9–15), but this is not decreased by actB neutralization (n = 6) (g). h MC were stimulated with TGF beta 1 or actA for 1 h, then treated with their type I receptor inhibitor SB431542 (50 uM). Restimulation with the same ligand shows that cells become refractory to TGF beta 1, but not actA (n = 4). *, **, ***, ****P < 0.05, 0.01, 0.001, 0.0001; one-way ANOVA with Tukey’s multiple comparisons post hoc test Image collected and cropped by CiteAb from the following open publication (https://pubmed.ncbi.nlm.nih.gov/36717814), licensed under a CC-BY license. Not internally tested by Novus Biologicals.
Smad3 [p Ser423, p Ser425] Antibody - BSA Free

Western Blot: Smad3 [p Ser423, p Ser425] Antibody - BSA Free [NBP1-77836] -

Mechanistic studies (I): Roflumilast prevents TGF beta 1-induced phospho-SMAD3 by the increase of PPM1A, the inhibition of reactive oxygen species (ROS) and phospho-ERK1/2-Protein Kinase A axis. Human keratinocytes were incubated for 30 min with vehicle or roflumilast (Rof, 100 nM) (A-F), the SMAD3 inhibitor (SIS3, 10uM) (A), the anti-oxidant N-acetyl-L-cysteine (NAC, 1 mM) (B, E), the PPM1A inhibitor sanguinarine (San, 3 uM) (D), the proteasome inhibitor MG132 (MG132, 5 uM) (E), the PKA inhibitor (KT5720, 2uM) (C), the ERK1/2 inhibitor (PD98059, 10uM) (F) or combinations as indicated. Next, keratinocytes were stimulated with TGF beta 1 (10 ng/ml) for 30 min and p-SMAD3 and PPM1A proteins were analysed by Western blotting. Data are shown from densitometry as the ratio of target protein compared to beta -actin of three independent experiments per condition. Results of the densitometry are presented as scatter dot blot with median and interquartile range values. P-values are based on Kruskal-Wallis test followed by the Dunn’s post-hoc test Image collected and cropped by CiteAb from the following open publication (https://pubmed.ncbi.nlm.nih.gov/39223490), licensed under a CC-BY license. Not internally tested by Novus Biologicals.
Smad3 [p Ser423, p Ser425] Antibody - BSA Free

Western Blot: Smad3 [p Ser423, p Ser425] Antibody - BSA Free [NBP1-77836] -

Activin A neutralization inhibits renal fibrosis in TGF beta 1-overexpressing mice. a TGF beta 1 transcript is increased in mice genetically engineered to overexpress TGF beta 1 (HH) compared with wild-type mice (WT) (n = 6–7, *p ≤ 0.05). b Serum actA is elevated in wild-type and HH mice after UUO. This is decreased by treatment with a neutralizing actA antibody (anti-actA) in HH mice. c Renal actA is increased after UUO, with a greater induction in HH mice. Both are attenuated by actA neutralization. Boxed areas are shown at higher magnification immediately below. ActA increases are seen particularly in tubular epithelial cells. d Renal alpha SMA, fibronectin (FN), pSmad3 and MRTF-A are increased after UUO and this is augmented in HH kidneys. Expression of all is attenuated by actA neutralization in both WT and HH kidneys. (n = 6–9) *, **, ***, ****P < 0.05, 0.01, 0.001, 0.0001; one-way ANOVA with Tukey’s multiple comparisons post hoc test where there are > 2 groups; t-test for 2 groups Image collected and cropped by CiteAb from the following open publication (https://pubmed.ncbi.nlm.nih.gov/36717814), licensed under a CC-BY license. Not internally tested by Novus Biologicals.
Smad3 [p Ser423, p Ser425] Antibody - BSA Free

Western Blot: Smad3 [p Ser423, p Ser425] Antibody - BSA Free [NBP1-77836] -

Mechanistic studies (I): Roflumilast prevents TGF beta 1-induced phospho-SMAD3 by the increase of PPM1A, the inhibition of reactive oxygen species (ROS) and phospho-ERK1/2-Protein Kinase A axis. Human keratinocytes were incubated for 30 min with vehicle or roflumilast (Rof, 100 nM) (A-F), the SMAD3 inhibitor (SIS3, 10uM) (A), the anti-oxidant N-acetyl-L-cysteine (NAC, 1 mM) (B, E), the PPM1A inhibitor sanguinarine (San, 3 uM) (D), the proteasome inhibitor MG132 (MG132, 5 uM) (E), the PKA inhibitor (KT5720, 2uM) (C), the ERK1/2 inhibitor (PD98059, 10uM) (F) or combinations as indicated. Next, keratinocytes were stimulated with TGF beta 1 (10 ng/ml) for 30 min and p-SMAD3 and PPM1A proteins were analysed by Western blotting. Data are shown from densitometry as the ratio of target protein compared to beta -actin of three independent experiments per condition. Results of the densitometry are presented as scatter dot blot with median and interquartile range values. P-values are based on Kruskal-Wallis test followed by the Dunn’s post-hoc test Image collected and cropped by CiteAb from the following open publication (https://pubmed.ncbi.nlm.nih.gov/39223490), licensed under a CC-BY license. Not internally tested by Novus Biologicals.
Smad3 [p Ser423, p Ser425] Antibody - BSA Free

Western Blot: Smad3 [p Ser423, p Ser425] Antibody - BSA Free [NBP1-77836] -

Specific activin A inhibition attenuates TGF beta 1-induced Smad3 activation and profibrotic responses in MC. a ELISA demonstrates that TGF beta 1 (24 h) increases actA and actB secretion (n = 3) to 19.5 ng/ml and 2.5 ng/ml, representing an 8.9- and 1.06-fold induction respectively. b TGF beta 1 increases actA in whole cell lysate by 1.8-fold (n = 3). c ActA (20 ng/ml) upregulates FN (n = 3–4), CTGF (n = 4) and alpha SMA (n = 6) at 48 h. d TGF beta 1 and actA both increase Smad3 transcriptional activity; no synergistic effect is seen (n = 6–12). e An actA neutralizing antibody attenuates TGF beta 1-induced FN (n = 5–6), alpha SMA (n = 5), CTGF (n = 5–6), and Smad3 activation (n = 10–12). f ActA neutralization decreases TGF beta 1-induced Smad3 transcriptional activity at 24 h (n = 9–15), but this is not decreased by actB neutralization (n = 6) (g). h MC were stimulated with TGF beta 1 or actA for 1 h, then treated with their type I receptor inhibitor SB431542 (50 uM). Restimulation with the same ligand shows that cells become refractory to TGF beta 1, but not actA (n = 4). *, **, ***, ****P < 0.05, 0.01, 0.001, 0.0001; one-way ANOVA with Tukey’s multiple comparisons post hoc test Image collected and cropped by CiteAb from the following open publication (https://pubmed.ncbi.nlm.nih.gov/36717814), licensed under a CC-BY license. Not internally tested by Novus Biologicals.
Smad3 [p Ser423, p Ser425] Antibody - BSA Free

Western Blot: Smad3 [p Ser423, p Ser425] Antibody - BSA Free [NBP1-77836] -

Activin inhibition attenuates TGF beta 1-induced fibrotic responses and Smad3 activation in MC. Activin inhibition with follistatin (FST) decreases TGF beta 1-induced: a FN, alpha SMA and CTGF upregulation at 48 h (n = 5), b Smad3 phosphorylation (pSmad3) at 24 h (n = 5), c Smad3 nuclear translocation as assessed using eGFP-Smad3 (n = 3; 25–30 cells quantified per treatment group) at 24 h, and d Smad3 transcriptional activity at 24 h (n = 8). e Time course experiments show increases in pSmad3 occur earlier (30–60 min) with TGF beta 1 (n = 4) compared with actA (n = 4) or actB (n = 3) (18–48 h). *, **, ***, ****P < 0.05, 0.01, 0.001, 0.0001; one-way ANOVA with Tukey’s multiple comparisons post hoc test Image collected and cropped by CiteAb from the following open publication (https://pubmed.ncbi.nlm.nih.gov/36717814), licensed under a CC-BY license. Not internally tested by Novus Biologicals.
Smad3 [p Ser423, p Ser425] Antibody - BSA Free

Western Blot: Smad3 [p Ser423, p Ser425] Antibody - BSA Free [NBP1-77836] -

Impact of PAD4 deficiency on TGF‐ beta signalling. (A) Activation of the canonical and non‐canonical pathway by TGF‐ beta was examined by Western blot. TGF‐ beta stimulation (10 ng/ml) for 2 h significantly increased protein levels of pSMAD2 and pSMAD3 in CFs independently on PAD4 deficiency. TGF‐ beta failed to activate STAT3 and Akt in PAD4−/− CFs. n = 6–8. Preincubation of WT CFs with the PAD4 inhibitor Cl‐amidine for 18 h abrogated TGF‐ beta ‐induced activation of Akt (B) and subsequent GSK‐3 beta phosphorylation (C). n = 3. (D) No TGF‐ beta ‐triggered phosphorylation of GSK‐3 beta was detected in PAD4−/− CFs. n = 3. *p < 0.05, **p < 0.01, ***p < 0.001 vs. control cells for A; #p < 0.05 for B and C Image collected and cropped by CiteAb from the following open publication (https://pubmed.ncbi.nlm.nih.gov/34523218), licensed under a CC-BY license. Not internally tested by Novus Biologicals.
Smad3 [p Ser423, p Ser425] Antibody - BSA Free

Western Blot: Smad3 [p Ser423, p Ser425] Antibody - BSA Free [NBP1-77836] -

Activin A facilitates TGF beta 1-induced type II receptor expression without altering TGF beta 1 receptor sensitivity in MC. a TGF beta 1 for 30 min increased TRII expression and Smad3 activation in whole cell lysate, and both were prevented by 24 h pretreatment with follistatin (n = 6). b There was no change in TRII transcript after 24 h of follistatin with or without TGF beta 1 for 30 min. c Pretreatment with an actA neutralizing antibody for 24 h inhibited acute (30 min) TGF beta 1-induced Smad3 activation and TRII upregulation (n = 6–7). These were similarly inhibited by downregulation of the actA type I receptor ALK4 with siRNA (d) (n = 3). e Pretreatment with actA (20 ng/ml) for 24 h did not affect acute TGF beta 1-induced Smad3 activation (n = 6). *, **, ****P < 0.05, 0.01, 0.0001; one-way ANOVA with Tukey’s multiple comparisons post hoc test Image collected and cropped by CiteAb from the following open publication (https://pubmed.ncbi.nlm.nih.gov/36717814), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Applications for Smad3 [p Ser423, p Ser425] Antibody - BSA Free

Application
Recommended Usage

ELISA

1:15000-1:30000

Flow Cytometry

1:10-1:1000

Immunohistochemistry

1:500

Immunohistochemistry-Paraffin

1:10-1:500

Single Cell Western

100 ug/ml

Western Blot

1:2000-1:20000
Application Notes
This affinity purified antibody has been tested for use in ELISA, immunohistochemistry, and western blot. Specific conditions for reactivity should be optimized by the end user. Expect a band approximately 48 kDa in size corresponding to phosphorylated Smad3 protein by western blotting in the appropriate stimulated tissue or cell lysate or extract. Less than 0.2% reactivity is observed against the non-phosphorylated form of the immunizing peptide. This antibody is phospho specific for dual phosphorylated pS423 and pS425 of Smad3. Stimulation with 2 ng/ml TGF-beta for 1 hour is suggested.

Reviewed Applications

Read 1 review rated 3 using NBP1-77836 in the following applications:

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Formulation, Preparation, and Storage

Purification

Immunogen affinity purified

Formulation

0.02 M Potassium Phosphate, 0.15 M Sodium Chloride, pH 7.2

Format

BSA Free

Preservative

0.01% Sodium Azide

Concentration

Please see the vial label for concentration. If unlisted please contact technical services.

Shipping

The product is shipped with polar packs. Upon receipt, store it immediately at the temperature recommended below.

Stability & Storage

Store at -20C short term. Aliquot and store at -80C long term. Avoid freeze-thaw cycles.

Background: Smad3

Smad3 (also known as Mothers against decapentaplegic homolog 3 Mothers against DPP homolog 3, Mad3, hMAD-3, JV15-2 or hSMAD3) is a transcriptional modulator activated by TGF-beta (transforming growth factor) and activin type 1 receptor kinase. These activators exert diverse effects on a wide array of cellular processes. The Smad proteins mediate much of the signaling responses induced by the TGF-b superfamily. Briefly, activated type I receptor phosphorylates receptor-activated Smads (R-Smads) at their c-terminal two extreme serines in the SSXS motif, e.g. Smad2 and Smad3 proteins in the TGF-b pathway, or Smad1, Smad5 or Smad8 in the BMP pathway. Then the phosphorylated R-Smad translocated into nucleus, where they regulate transcription of target genes. Based on microarray and animal model experiments, Smad3 accounts for at least 80% of all TGF-b-mediated response.

Long Name

Mothers Against DPP Homolog 3

Alternate Names

DKFZp586N0721, DKFZp686J10186, hMAD-3, hSMAD3, HsT17436, JV15-2MGC60396, MAD homolog 3, mad protein homolog, MAD, mothers against decapentaplegic homolog 3, MAD, mothers against decapentaplegic homolog 3 (Drosophila), mad3, MADH3mad homolog JV15-2, mothers against decapentaplegic homolog 3, Mothers against DPP homolog 3, SMA- and MAD-related protein 3, SMAD 3, SMAD family member 3HSPC193, SMAD, mothers against DPP homolog 3, SMAD, mothers against DPP homolog 3 (Drosophila), Smad3, pSMAD

Gene Symbol

SMAD3

UniProt

P84022, NC_000015.9 (Human)

Additional Smad3 Products

Product Documents for Smad3 [p Ser423, p Ser425] Antibody - BSA Free

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Product Specific Notices for Smad3 [p Ser423, p Ser425] Antibody - BSA Free

This product is for research use only and is not approved for use in humans or in clinical diagnosis. Primary Antibodies are guaranteed for 1 year from date of receipt.

Citations for Smad3 [p Ser423, p Ser425] Antibody - BSA Free

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  • Smad3 [p Ser423, p Ser425] Antibody
    Name: Anonymous
    Application: Immunohistochemistry-Frozen
    Sample Tested: Retina
    Species: Feline
    Verified Customer | Posted 08/15/2017
    Green-NBP1-77836 at 1:500 dilution, Blue-DAPI.
    Smad3 [p Ser423, p Ser425] Antibody - BSA Free NBP1-77836

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FAQs for Smad3 [p Ser423, p Ser425] Antibody - BSA Free

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  • Q: I was wondering if you can recommend any primary polyclonal Smad3 antibody (reactivity: human) for gel supershifts?

    A: We do provide a wide range of Smad3 antibodies, but unfortunately none of them have been tested for gel shift assay, so we can't guarantee they will work for an application never tested before.

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