Antibody data
- Antibody Data
- Antigen structure
- References [1]
- Comments [0]
- Validations
- Immunohistochemistry [7]
- Other assay [1]
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- Product number
- MA5-26050 - Provider product page
- Provider
- Invitrogen Antibodies
- Product name
- Rhotekin Monoclonal Antibody (OTI2E9)
- Antibody type
- Monoclonal
- Antigen
- Recombinant full-length protein
- Reactivity
- Human
- Host
- Mouse
- Isotype
- IgG
- Antibody clone number
- OTI2E9
- Vial size
- 100 µL
- Concentration
- 1 mg/mL
- Storage
- -20° C, Avoid Freeze/Thaw Cycles
Submitted references S100A4 is activated by RhoA and catalyses the polymerization of non-muscle myosin, adhesion complex assembly and contraction in airway smooth muscle.
Zhang W, Gunst SJ
The Journal of physiology 2020 Oct;598(20):4573-4590
The Journal of physiology 2020 Oct;598(20):4573-4590
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Supportive validation
- Submitted by
- Invitrogen Antibodies (provider)
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- Experimental details
- Immunohistochemistry was performed on paraffin-embedded human bladder tissue. To expose target proteins, 10mM citric buffer, pH6.0, 120°C for 3min was used. Following antigen retrieval, tissues were probed with a RTKN monoclonal antibody (Product # MA5-26050).
- Submitted by
- Invitrogen Antibodies (provider)
- Main image
- Experimental details
- Immunohistochemistry was performed on paraffin-embedded human pancreas tissue. To expose target proteins, 10mM citric buffer, pH6.0, 120°C for 3min was used. Following antigen retrieval, tissues were probed with a RTKN monoclonal antibody (Product # MA5-26050).
- Submitted by
- Invitrogen Antibodies (provider)
- Main image
- Experimental details
- Immunohistochemistry was performed on paraffin-embedded human kidney tissue. To expose target proteins, 10mM citric buffer, pH6.0, 120°C for 3min was used. Following antigen retrieval, tissues were probed with a RTKN monoclonal antibody (Product # MA5-26050).
- Submitted by
- Invitrogen Antibodies (provider)
- Main image
- Experimental details
- Immunohistochemistry was performed on paraffin-embedded carcinoma of human thyroid tissue. To expose target proteins, 10mM citric buffer, pH6.0, 120°C for 3min was used. Following antigen retrieval, tissues were probed with a RTKN monoclonal antibody (Product # MA5-26050).
- Submitted by
- Invitrogen Antibodies (provider)
- Main image
- Experimental details
- Immunohistochemistry was performed on paraffin-embedded carcinoma of human prostate tissue. To expose target proteins, 10mM citric buffer, pH6.0, 120°C for 3min was used. Following antigen retrieval, tissues were probed with a RTKN monoclonal antibody (Product # MA5-26050).
- Submitted by
- Invitrogen Antibodies (provider)
- Main image
- Experimental details
- Immunohistochemistry was performed on paraffin-embedded human liver tissue. To expose target proteins, 10mM citric buffer, pH6.0, 120°C for 3min was used. Following antigen retrieval, tissues were probed with a RTKN monoclonal antibody (Product # MA5-26050).
- Submitted by
- Invitrogen Antibodies (provider)
- Main image
- Experimental details
- Immunohistochemistry was performed on paraffin-embedded human tonsil tissue. To expose target proteins, 10mM citric buffer, pH6.0, 120°C for 3min was used. Following antigen retrieval, tissues were probed with a RTKN monoclonal antibody (Product # MA5-26050).
Supportive validation
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- Invitrogen Antibodies (provider)
- Main image
- Experimental details
- 5 Figure Rhotekin couples RhoA to S100A4 and NM myosin II in SM cells and tissues stimulated with ACh A , rhotekin (RTKN) was immunoprecipitated from tissue extracts and immunocomplexes were blotted for RhoA, S100A4, RTKN and NM myosin IIA. Stimulation for 5 min with 10 -5 M ACh significantly increased the coprecipitation of NM myosin IIA ( n = 6, p = 0.0070), RhoA ( n = 3, p = 0.0359) and S100A4 ( n = 9, p = 0.0001) with RTKN. B , in situ PLA was used to determine the interaction of RTKN and RhoA, S100A4 and NM myosin IIA in freshly dissociated tracheal SM cells. Stimulation with ACh caused a significant increase in the number of PLA complexes between all four proteins (RTKN-RhoA, n = 20, p = 0.0001; RTKN-S100A4, n = 20, p = 0.0001; RTKN-NM myosin IIA, n = 31, p = 0.0001). C , tracheal SM tissues were treated with RTKN siRNA. Depletion of RTKN significantly inhibited protein expression ( n = 10, p = 0.0001) and also inhibited tension development in response to 10 -5 M ACh stimulation ( n = 16, p = 0.0001). D , PLA shows interactions between S100A4 and RhoA in cells dissociated from sham-treated tissues and from RTKN-depleted tissues. ACh stimulation of sham-treated cells resulted in a significant increase in the interactions between S100A4 and RhoA (US, n = 16; ACh, n = 20). RTKN depletion inhibited the ACh-induced increase of the interaction between S100A4 and RhoA ( p = 0.0001) (US, n = 18; ACh, n = 19). Data analysed by a paired Student's t test ( A and C ), an unpaired S