|Tested species reactivity||Human, Rat|
|Published species reactivity||Rat, Human, Mouse, Not Applicable|
|Host / Isotype||Mouse / IgG1, kappa|
|Immunogen||Purified recombinant full-length human paxillin protein|
|Storage buffer||PBS, pH 7.4, with 0.2% BSA|
|Contains||0.09% sodium azide|
|Storage Conditions||4° C|
|Tested Applications||Dilution *|
|Immunofluorescence (IF)||Assay Dependent|
|Immunohistochemistry (Paraffin) (IHC (P))||1-2 µg/ml|
|Immunoprecipitation (IP)||2 µg/ml|
|Western Blot (WB)||1-2 µg/ml|
* Suggested working dilutions are given as a guide only. It is recommended that the user titrate the product for use in their own experiment using appropriate negative and positive controls.
MA5-13356 targets Paxillin in IF, IHC (P), IP, and WB applications and shows reactivity with Human and Rat samples.
The MA5-13356 immunogen is purified recombinant full-length human paxillin protein.
Paxillin is a focal adhesion protein and a substrate for several tyrosine kinases such as src, FAK, and p210BRC/ABL. The tyrosine phosphorylation of paxillin is affected by conditions that change cell-cell adhesion. Paxillin associates tightly with FAK and Crk through its SH2 domain. This interaction is independent of the extracellular matrix. Although paxillin was initially discovered in fibroblasts, its phosphorylation may also be important during neurite extension during differentiation.
For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.
Targeting focal adhesion turnover in invasive breast cancer cells by the purine derivative reversine.
MA5-13356 was used in western blot to study the beneficial effects of reversine-mediated disruption of focal adhesion turnover on breast cancer metastasis
|Bijian K,Lougheed C,Su J,Xu B,Yu H,Wu JH,Riccio K,Alaoui-Jamali MA||British journal of cancer (109:2810)||2013|
Extraribosomal function of metallopanstimulin-1: reducing paxillin in head and neck squamous cell carcinoma and inhibiting tumor growth.
MA5-13356 was used in western blot to investigate the effect of metallopanstimulin-1 on tumor growth and gene expression
|Dai Y,Pierson SE,Dudney WC,Stack BC||International journal of cancer (126:611)||2010|
|Not Applicable||Not Cited||
Presenilin 1 affects focal adhesion site formation and cell force generation via c-Src transcriptional and posttranslational regulation.
MA5-13356 was used in western blot to assess the function of presenilins in the cell-matrix interactions of mouse embryonic fibroblasts
|Waschbüsch D,Born S,Niediek V,Kirchgessner N,Tamboli IY,Walter J,Merkel R,Hoffmann B||The Journal of biological chemistry (284:10138)||2009|
Smooth muscle alpha-actin deficiency in myofibroblasts leads to enhanced renal tissue fibrosis.
MA5-13356 was used in western blot to examine the role of smooth muscle alpha-actin deficiency in renal tissue fibrosis
|Takeji M,Moriyama T,Oseto S,Kawada N,Hori M,Imai E,Miwa T||The Journal of biological chemistry (281:40193)||2006|
Decreased ezrin and paxillin expression in human urothelial bladder tumors correlate with tumor progression.
MA5-13356 was used in immunohistochemistry to study the clinical significance of ezrin and paxillin downregulation in human urothelial bladder tumors
|Athanasopoulou A,Aroukatos P,Nakas D,Repanti M,Papadaki H,Bravou V||Urologic oncology (31:836)||2013|
Expression of claudin, paxillin and FRA-1 in non-nodular breast lesions in association with microcalcifications.
MA5-13356 was used in immunohistochemistry to study non-nodular breast lesions for the expression of claudin, paxillin and FRA-1
|Kandelman JD,Waitzberg AF,Szejnfeld J,Smith RL||Sao Paulo medical journal = Revista paulista de medicina (131:71)||2013|
The influence of tubular phenotypic changes on the development of diffuse interstitial fibrosis in renal allografts.
MA5-13356 was used in immunohistochemistry to study the role of tubular phenotypic changes in the development of diffuse interstitial fibrosis in renal allografts
|Özdemir BH,Özdemir AA,Colak T,Sezer S,Haberal M||Transplantation proceedings (43:527)||2011|
Paxillin expression and amplification in early lung lesions of high-risk patients, lung adenocarcinoma and metastatic disease.
MA5-13356 was used in immunohistochemistry to study paxillin expression and amplification in early lung lesions and its role in lung carcinogenesis
|Mackinnon AC,Tretiakova M,Henderson L,Mehta RG,Yan BC,Joseph L,Krausz T,Husain AN,Reid ME,Salgia R||Journal of clinical pathology (64:16)||2011|
Cyclic strain modulates migration and proliferation of vascular smooth muscle cells via Rho-GDIalpha, Rac1, and p38 pathway.
MA5-13356 was used in immunohistochemistry to study the mechanism for the induction of vascular smooth muscle cell migration and proliferation by cyclic strain
|Qi YX,Qu MJ,Yan ZQ,Zhao D,Jiang XH,Shen BR,Jiang ZL||Journal of cellular biochemistry (109:906)||2010|
Focal adhesion plaque associated cytoskeletons are involved in the invasion and metastasis of human colorectal carcinoma.
MA5-13356 was used in immunohistochemistry to investigate the involvement of focal adhesion plaque associated cytoskeletons in the invasion and metastasis of colorectal carcinoma
|Yang HJ,Chen JZ,Zhang WL,Ding YQ||Cancer investigation (28:127)||2010|
The expression of the cytoskeletal focal adhesion protein paxillin in breast cancer correlates with HER2 overexpression and may help predict response to chemotherapy: a retrospective immunohistochemical study.
MA5-13356 was used in immunohistochemistry to investigate the association between paxillin expression and HER2 expression in breast cancer patients
|Short SM,Yoder BJ,Tarr SM,Prescott NL,Laniauskas S,Coleman KA,Downs-Kelly E,Pettay JD,Choueiri TK,Crowe JP,Tubbs RR,Budd TG,Hicks DG||The breast journal (13:130)||2007|
Vascular smooth muscle cells promote endothelial cell adhesion via microtubule dynamics and activation of paxillin and the extracellular signal-regulated kinase (ERK) pathway in a co-culture system.
MA5-13356 was used in immunocytochemistry to investigate the importance of vascular smooth muscle cells in endothelial cell adhesion
|Wang YH,Yan ZQ,Shen BR,Zhang L,Zhang P,Jiang ZL||European journal of cell biology (88:701)||2009|