Testing Data
(Staining of mouse spleen with Hamster anti Mouse CD81: Alexa Fluor 647 (MBS212342A647))
Hamster CD81 Monoclonal Antibody | anti-CD81 antibody
HAMSTER ANTI MOUSE CD81:FITC
Purified IgG conjugated to Fluorescein Isothiocyanate Isomer 1 (FITC) - liquid
1% Bovine Serum Albumin
Preparation
Fusion Partners
Shelf Life: 18 months from date of despatch.
Testing Data
(Staining of mouse spleen with Hamster anti Mouse CD81: Alexa Fluor 647 (MBS212342A647))
Testing Data
(Staining of mouse spleen with Hamster anti Mouse CD81: Alexa Fluor 647 (MBS212342A647))
Testing Data
(Staining of mouse spleen cells with Hamster anti Mouse CD81:FITC)
Testing Data
(Staining of mouse spleen cells with Hamster anti Mouse CD81:FITC)
Testing Data
(Published customer image: Fluvastatin and simvastatin increase CD9 and CD81 levels in RAW264.7 cells.(A) RAW264.7 cells were cultured for 24 h in the absence or presence of increasing concentrations of fluvastatin (Fluv) or simvastatin (Simv). The cells were lysed, and levels of CD9, CD63, and CD81 were examined by immunoblotting. Anti-actin blots show that comparable amounts of protein were loaded in each lane. (B) RAW264.7 cells were untreated (-) or cultured in the absence or presence of increasing concentrations of fluvastatin or simvastatin and stimulated for 24 h with 0.1 ug/ml LPS (+). Levels of CD9, CD63, and CD81 were examined by immunoblotting. Note that LPS downregulates CD9 and CD81 in the absence of statins (arrowheads). (C) RAW264.7 cells were cultured in the absence (-) or presence of 3 uM fluvastatin (+), and unstimulated (-) or stimulated for 24 h with 1 ug/ml LPS (+). mRNA levels of CD9 and CD81 were examined by reverse transcription PCR. GAPDH is an internal loading control. (D) RAW264.7 cells were cultured in the absence or presence of fluvastatin, and unstimulated or stimulated with LPS. Control (Cont) was an untreated culture. mRNA levels of CD9 and CD81 were examined by real-time PCR. Data shown are from one representative of three similar experiments. (E) Human monocytic THP-1 cells were treated for 4 h with 1 ug/ml phorbol 12-myristate 13-acetate, allowed to attach to a plate, and then cultured in the absence or presence of increasing concentrations of simvastatin. Levels of CD9, CD63, and CD81 were examined by immunoblotting. (F) Mouse 3T3 fibroblasts were cultured in the absence or presence of increasing concentrations of simvastatin. Levels of CD9, CD63, and CD81 were examined by immunoblotting.From: Jin Y, Tachibana I, Takeda Y, He P, Kang S, et al. (2013) Statins Decrease Lung Inflammation in Mice by Upregulating Tetraspanin CD9 in Macrophages. PLoS ONE 8(9): e73706.)
Testing Data
(Published customer image: Fluvastatin and simvastatin increase CD9 and CD81 levels in RAW264.7 cells.(A) RAW264.7 cells were cultured for 24 h in the absence or presence of increasing concentrations of fluvastatin (Fluv) or simvastatin (Simv). The cells were lysed, and levels of CD9, CD63, and CD81 were examined by immunoblotting. Anti-actin blots show that comparable amounts of protein were loaded in each lane. (B) RAW264.7 cells were untreated (-) or cultured in the absence or presence of increasing concentrations of fluvastatin or simvastatin and stimulated for 24 h with 0.1 ug/ml LPS (+). Levels of CD9, CD63, and CD81 were examined by immunoblotting. Note that LPS downregulates CD9 and CD81 in the absence of statins (arrowheads). (C) RAW264.7 cells were cultured in the absence (-) or presence of 3 uM fluvastatin (+), and unstimulated (-) or stimulated for 24 h with 1 ug/ml LPS (+). mRNA levels of CD9 and CD81 were examined by reverse transcription PCR. GAPDH is an internal loading control. (D) RAW264.7 cells were cultured in the absence or presence of fluvastatin, and unstimulated or stimulated with LPS. Control (Cont) was an untreated culture. mRNA levels of CD9 and CD81 were examined by real-time PCR. Data shown are from one representative of three similar experiments. (E) Human monocytic THP-1 cells were treated for 4 h with 1 ug/ml phorbol 12-myristate 13-acetate, allowed to attach to a plate, and then cultured in the absence or presence of increasing concentrations of simvastatin. Levels of CD9, CD63, and CD81 were examined by immunoblotting. (F) Mouse 3T3 fibroblasts were cultured in the absence or presence of increasing concentrations of simvastatin. Levels of CD9, CD63, and CD81 were examined by immunoblotting.From: Jin Y, Tachibana I, Takeda Y, He P, Kang S, et al. (2013) Statins Decrease Lung Inflammation in Mice by Upregulating Tetraspanin CD9 in Macrophages. PLoS ONE 8(9): e73706.)
Testing Data
(Published customer image: Statins transfer CD14 from lipid rafts into CD9-enriched microdomains. (A) RAW264.7 cells were stimulated with 0.1 ug/ml LPS and, after the indicated times, the cells were lysed and protein levels were examined by immunoblotting. Anti-actin blots show that comparable amounts of protein were loaded in each lane. (B) RAW264.7 cells were untreated (-) or cultured for 24 h in the absence (-) or presence of 5 uM fluvastatin (Fluv) or simvastatin (Simv) (+) and stimulated for 2 h with 1 ug/ml LPS (+). Proteins in whole-cell lysate (WCL) and CD14 protein in immunoprecipitates (IP) with anti-TLR4 Ab were immunoblotted (IB). (C) RAW264.7 cells were treated as in B. Lysates of untreated (C, control) cultures or LPS-stimulated cultures in the absence (L) or presence of fluvastatin (FL) or simvastatin (SL) were fractionated by sucrose density gradients, and protein distributions were visualized by immunoblotting. The intensities of blots were quantified by densitometry, and percentages of density units of light membrane (LM) fractions are displayed to the right of the blots. Data shown are from one representative of three similar experiments. (D) Immunoblots of CD9 and CD81 proteins in whole-cell lysates and in immunoprecipitates with control IgG or anti-CD14 mAb. (E) Immunoblots of CD9 and CD81 proteins in whole-cell lysates and in immunoprecipitates with control IgG or anti-CD14 mAb from pooled LM fractions (4 and 5) and dense (D) fractions (9 and 10). In the presence of statins, more CD14/CD9 complexes were formed in dense fractions (arrowheads).From: Jin Y, Tachibana I, Takeda Y, He P, Kang S, et al. (2013) Statins Decrease Lung Inflammation in Mice by Upregulating Tetraspanin CD9 in Macrophages. PLoS ONE 8(9): e73706.)
Testing Data
(Published customer image: Statins transfer CD14 from lipid rafts into CD9-enriched microdomains. (A) RAW264.7 cells were stimulated with 0.1 ug/ml LPS and, after the indicated times, the cells were lysed and protein levels were examined by immunoblotting. Anti-actin blots show that comparable amounts of protein were loaded in each lane. (B) RAW264.7 cells were untreated (-) or cultured for 24 h in the absence (-) or presence of 5 uM fluvastatin (Fluv) or simvastatin (Simv) (+) and stimulated for 2 h with 1 ug/ml LPS (+). Proteins in whole-cell lysate (WCL) and CD14 protein in immunoprecipitates (IP) with anti-TLR4 Ab were immunoblotted (IB). (C) RAW264.7 cells were treated as in B. Lysates of untreated (C, control) cultures or LPS-stimulated cultures in the absence (L) or presence of fluvastatin (FL) or simvastatin (SL) were fractionated by sucrose density gradients, and protein distributions were visualized by immunoblotting. The intensities of blots were quantified by densitometry, and percentages of density units of light membrane (LM) fractions are displayed to the right of the blots. Data shown are from one representative of three similar experiments. (D) Immunoblots of CD9 and CD81 proteins in whole-cell lysates and in immunoprecipitates with control IgG or anti-CD14 mAb. (E) Immunoblots of CD9 and CD81 proteins in whole-cell lysates and in immunoprecipitates with control IgG or anti-CD14 mAb from pooled LM fractions (4 and 5) and dense (D) fractions (9 and 10). In the presence of statins, more CD14/CD9 complexes were formed in dense fractions (arrowheads).From: Jin Y, Tachibana I, Takeda Y, He P, Kang S, et al. (2013) Statins Decrease Lung Inflammation in Mice by Upregulating Tetraspanin CD9 in Macrophages. PLoS ONE 8(9): e73706.)
Testing Data
(Published customer image: The anti-inflammatory effects of statins are CD9-dependent. (A) BMDMs from WT mice were cultured for 24 h in the absence (-) or presence of 3 uM fluvastatin (Fluv) (+), and unstimulated (-) or stimulated for 24 h with 1 ug/ml LPS (+). The cells were lysed, and levels of CD9 and CD81 were examined by immunoblotting. Anti-actin blots show that comparable amounts of protein were loaded in each lane. (B) BMDMs from WT and CD9 KO mice were cultured in the absence or presence of the indicated concentrations of fluvastatin, and stimulated for 18 h with 10 ug/ml LPS (+). Activities of MMP-9 in culture supernatants were analyzed by gelatin zymography. (C) BMDMs from WT and CD9 KO mice were cultured in the absence (vehicle) or presence of 10 uM fluvastatin or simvastatin (Simv), and unstimulated (-) or stimulated for 18 h with 1 ug/ml LPS (+). Concentrations of TNF-a in culture supernatants were measured by ELISA. Each bar represents the mean +/- SEM. ?P < 0.05; ? ? P < 0.01.From: Jin Y, Tachibana I, Takeda Y, He P, Kang S, et al. (2013) Statins Decrease Lung Inflammation in Mice by Upregulating Tetraspanin CD9 in Macrophages. PLoS ONE 8(9): e73706.)
Testing Data
(Published customer image: The anti-inflammatory effects of statins are CD9-dependent. (A) BMDMs from WT mice were cultured for 24 h in the absence (-) or presence of 3 uM fluvastatin (Fluv) (+), and unstimulated (-) or stimulated for 24 h with 1 ug/ml LPS (+). The cells were lysed, and levels of CD9 and CD81 were examined by immunoblotting. Anti-actin blots show that comparable amounts of protein were loaded in each lane. (B) BMDMs from WT and CD9 KO mice were cultured in the absence or presence of the indicated concentrations of fluvastatin, and stimulated for 18 h with 10 ug/ml LPS (+). Activities of MMP-9 in culture supernatants were analyzed by gelatin zymography. (C) BMDMs from WT and CD9 KO mice were cultured in the absence (vehicle) or presence of 10 uM fluvastatin or simvastatin (Simv), and unstimulated (-) or stimulated for 18 h with 1 ug/ml LPS (+). Concentrations of TNF-a in culture supernatants were measured by ELISA. Each bar represents the mean +/- SEM. ?P < 0.05; ? ? P < 0.01.From: Jin Y, Tachibana I, Takeda Y, He P, Kang S, et al. (2013) Statins Decrease Lung Inflammation in Mice by Upregulating Tetraspanin CD9 in Macrophages. PLoS ONE 8(9): e73706.)
Testing Data
(Published customer image: Density fractionation of EVs. The figure shows sucrose gradients of EVs preparations from MLP29 (A) and RH (B). Aliquots of these fractions were used for RNA extraction and protein extraction; the most abundant transcripts were found in the fractions containing typical exosomal markers (Tsg101 or Aip1). RH preparations showed more diversity, with vesicle populations fractionating at different densities.From: Royo F, Schlangen K, Palomo L, Gonzalez E, Conde-Vancells J, et al. (2013) Transcriptome of Extracellular Vesicles Released by Hepatocytes. PLoS ONE 8(7): e68693.)
Testing Data
(Published customer image: Density fractionation of EVs. The figure shows sucrose gradients of EVs preparations from MLP29 (A) and RH (B). Aliquots of these fractions were used for RNA extraction and protein extraction; the most abundant transcripts were found in the fractions containing typical exosomal markers (Tsg101 or Aip1). RH preparations showed more diversity, with vesicle populations fractionating at different densities.From: Royo F, Schlangen K, Palomo L, Gonzalez E, Conde-Vancells J, et al. (2013) Transcriptome of Extracellular Vesicles Released by Hepatocytes. PLoS ONE 8(7): e68693.)
Testing Data
(Published customer image: Screening of a drug library for agents that upregulate CD9 or CD81 in RAW264.7 macrophages. (A) RAW264.7 cells were cultured for 24 h in the absence (V, vehicle alone) and presence of each drug (10 uM). The cells were lysed, and levels of CD9 and CD81 were examined by immunoblotting. Blots of results with fluvastatin (Fluv) and simvastatin (Simv) are shown. Anti-actin blots show that comparable amounts of protein were loaded in each lane. (B) After testing 1,165 drugs, levels of CD9 and CD81 relative to actin were quantified by densitometry. Fold changes of the expression levels compared with vehicle alone were calculated and plotted. Drugs that increased the level of either CD9 or CD81 more than 1.5-fold compared with vehicle alone were regarded as positive. Correlation between fold changes in CD9 and CD81 levels was analyzed using Pearson's correlation coefficient. (C) RAW264.7 cells were cultured in the absence (V) or presence of multiple statins (10 uM) and levels of CD9 and CD81 were examined by immunoblotting. The statins are arranged in order of decreasing lipophilicity. Ceri, cerivastatin; Simv, simvastatin; Fluv, fluvastatin; Ator, atorvastatin; Rosu, rosuvastatin; Prav, pravastatin. (D) RAW264.7 cells were cultured in the absence (shaded histograms) or presence (10 uM) of fluvastatin (open red histograms) and simvastatin (open blue histograms). Surface levels of CD9, CD63, CD81, and the integrin beta1 subunit were analyzed by flow cytometry.From: Jin Y, Tachibana I, Takeda Y, He P, Kang S, et al. (2013) Statins Decrease Lung Inflammation in Mice by Upregulating Tetraspanin CD9 in Macrophages. PLoS ONE 8(9): e73706.)
Testing Data
(Published customer image: Screening of a drug library for agents that upregulate CD9 or CD81 in RAW264.7 macrophages. (A) RAW264.7 cells were cultured for 24 h in the absence (V, vehicle alone) and presence of each drug (10 uM). The cells were lysed, and levels of CD9 and CD81 were examined by immunoblotting. Blots of results with fluvastatin (Fluv) and simvastatin (Simv) are shown. Anti-actin blots show that comparable amounts of protein were loaded in each lane. (B) After testing 1,165 drugs, levels of CD9 and CD81 relative to actin were quantified by densitometry. Fold changes of the expression levels compared with vehicle alone were calculated and plotted. Drugs that increased the level of either CD9 or CD81 more than 1.5-fold compared with vehicle alone were regarded as positive. Correlation between fold changes in CD9 and CD81 levels was analyzed using Pearson's correlation coefficient. (C) RAW264.7 cells were cultured in the absence (V) or presence of multiple statins (10 uM) and levels of CD9 and CD81 were examined by immunoblotting. The statins are arranged in order of decreasing lipophilicity. Ceri, cerivastatin; Simv, simvastatin; Fluv, fluvastatin; Ator, atorvastatin; Rosu, rosuvastatin; Prav, pravastatin. (D) RAW264.7 cells were cultured in the absence (shaded histograms) or presence (10 uM) of fluvastatin (open red histograms) and simvastatin (open blue histograms). Surface levels of CD9, CD63, CD81, and the integrin beta1 subunit were analyzed by flow cytometry.From: Jin Y, Tachibana I, Takeda Y, He P, Kang S, et al. (2013) Statins Decrease Lung Inflammation in Mice by Upregulating Tetraspanin CD9 in Macrophages. PLoS ONE 8(9): e73706.)
Testing Data
(Published customer image: Blockade of the mevalonate pathway increases CD9 and CD81. (A) RAW264.7 cells were untreated (-) or treated for 48 h with 50 ng/ml TSA (+) in the absence (-) or presence of 50 uM theophylline or 0.5 uM fluvastatin (Fluv) (+). The cells were lysed, and levels of CD9 and CD81 were examined by immunoblotting. Anti-actin blots show that comparable amounts of protein were loaded in each lane. (B) The mevalonate pathway and inhibitors. n-BP, nitrogenous bisphosphonate. (C) RAW264.7 cells were cultured for 24 h in the presence of indicated concentrations of fluvastatin, simvastatin (Simv), zoledronate (Zol), or risedronate (Ris). Levels of CD9 and CD81 were examined by immunoblotting. (D) RAW264.7 cells were cultured for 24 h in the absence (V, vehicle alone) or presence of mevalonate (Mev), farnesyl pyrophosphate (FPP), squalene (Squ), or geranylgeranyl pyrophosphate (GGPP). Although the actin level in the GGPP lane appears to be lower, an equal amount of protein was loaded. (E) RAW264.7 cells were cultured for 24 h in the absence (V) or presence of fluvastatin, zoledronate, farnesyl transferase inhibitor (FTI), or geranylgeranyl transferase inhibitor (GGTI). (F) RAW264.7 cells were untreated (-) or treated with fluvastatin (+) in the absence (V) or presence of mevalonate, FPP, squalene, or GGPP. (G) RAW264.7 cells were untreated (-) or treated with zoledronate (+) in the absence (V) or presence of mevalonate, FPP, squalene, or GGPP. (H) RAW264.7 cells were untreated (-) or treated with fluvastatin (+) in the absence (V) or presence of mevalonate, FPP, squalene, or GGPP and stimulated for 15 min with 0.1 ug/ml LPS (+). The cells were lysed, and levels of I?Ba were examined by immunoblotting. (I) RAW264.7 cells were cultured for 24 h in the indicated concentrations of HA1077. Levels of CD9 and CD81 were examined by immunoblotting.From: Jin Y, Tachibana I, Takeda Y, He P, Kang S, et al. (2013) Statins Decrease Lung Inflammation in Mice by Upregulating Tetraspanin CD9 in Macrophages. PLoS ONE 8(9): e73706.)
Testing Data
(Published customer image: Blockade of the mevalonate pathway increases CD9 and CD81. (A) RAW264.7 cells were untreated (-) or treated for 48 h with 50 ng/ml TSA (+) in the absence (-) or presence of 50 uM theophylline or 0.5 uM fluvastatin (Fluv) (+). The cells were lysed, and levels of CD9 and CD81 were examined by immunoblotting. Anti-actin blots show that comparable amounts of protein were loaded in each lane. (B) The mevalonate pathway and inhibitors. n-BP, nitrogenous bisphosphonate. (C) RAW264.7 cells were cultured for 24 h in the presence of indicated concentrations of fluvastatin, simvastatin (Simv), zoledronate (Zol), or risedronate (Ris). Levels of CD9 and CD81 were examined by immunoblotting. (D) RAW264.7 cells were cultured for 24 h in the absence (V, vehicle alone) or presence of mevalonate (Mev), farnesyl pyrophosphate (FPP), squalene (Squ), or geranylgeranyl pyrophosphate (GGPP). Although the actin level in the GGPP lane appears to be lower, an equal amount of protein was loaded. (E) RAW264.7 cells were cultured for 24 h in the absence (V) or presence of fluvastatin, zoledronate, farnesyl transferase inhibitor (FTI), or geranylgeranyl transferase inhibitor (GGTI). (F) RAW264.7 cells were untreated (-) or treated with fluvastatin (+) in the absence (V) or presence of mevalonate, FPP, squalene, or GGPP. (G) RAW264.7 cells were untreated (-) or treated with zoledronate (+) in the absence (V) or presence of mevalonate, FPP, squalene, or GGPP. (H) RAW264.7 cells were untreated (-) or treated with fluvastatin (+) in the absence (V) or presence of mevalonate, FPP, squalene, or GGPP and stimulated for 15 min with 0.1 ug/ml LPS (+). The cells were lysed, and levels of I?Ba were examined by immunoblotting. (I) RAW264.7 cells were cultured for 24 h in the indicated concentrations of HA1077. Levels of CD9 and CD81 were examined by immunoblotting.From: Jin Y, Tachibana I, Takeda Y, He P, Kang S, et al. (2013) Statins Decrease Lung Inflammation in Mice by Upregulating Tetraspanin CD9 in Macrophages. PLoS ONE 8(9): e73706.)
Testing Data
(Staining of mouse spleen with Hamster anti Mouse CD81: Alexa Fluor 488 (MBS212342A488))
Testing Data
(Staining of mouse spleen with Hamster anti Mouse CD81: Alexa Fluor 488 (MBS212342A488))
NCBI and Uniprot Product Information
Uniprot Description
CD81: May play an important role in the regulation of lymphoma cell growth. Interacts with a 16-kDa Leu-13 protein to form a complex possibly involved in signal transduction. May act as the viral receptor for HCV. Defects in CD81 are the cause of immunodeficiency common variable type 6 (CVID6); also called antibody deficiency due to CD81 defect. CVID6 is a primary immunodeficiency characterized by antibody deficiency, hypogammaglobulinemia, recurrent bacterial infections and an inability to mount an antibody response to antigen. The defect results from a failure of B-cell differentiation and impaired secretion of immunoglobulins; the numbers of circulating B-cells is usually in the normal range, but can be low. Belongs to the tetraspanin (TM4SF) family.
Protein type: Membrane protein, integral; Membrane protein, multi-pass
Cellular Component: focal adhesion; membrane; integral to plasma membrane; apical plasma membrane; integral to membrane; immunological synapse; vesicle
Molecular Function: protein binding
Biological Process: protein localization; positive regulation of peptidyl-tyrosine phosphorylation; activation of MAPK activity; positive regulation of 1-phosphatidylinositol 4-kinase activity; positive regulation of cell proliferation; phosphatidylinositol biosynthetic process; positive regulation of B cell proliferation; phosphatidylinositol metabolic process; positive regulation of cell growth; regulation of cell proliferation
Research Articles on CD81
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Product Notes
The CD81 cd81 (Catalog #AAA210783) is an Antibody produced from Hamster and is intended for research purposes only. The product is available for immediate purchase. AAA Biotech's CD81 can be used in a range of immunoassay formats including, but not limited to, Flow cytometry (FC/FACS). Flow Cytometry: Use 10ul of the suggested working dilution to label 106 cells in 100ul. The Fc region of monoclonal antibodies may bind non-specifically to cells expressing low affinity Fc receptors. This may be reduced by using SeroBlock FcR. Researchers should empirically determine the suitability of the CD81 cd81 for an application not listed in the data sheet. Researchers commonly develop new applications and it is an integral, important part of the investigative research process. It is sometimes possible for the material contained within the vial of "CD81, Monoclonal Antibody" to become dispersed throughout the inside of the vial, particularly around the seal of said vial, during shipment and storage. We always suggest centrifuging these vials to consolidate all of the liquid away from the lid and to the bottom of the vial prior to opening. Please be advised that certain products may require dry ice for shipping and that, if this is the case, an additional dry ice fee may also be required.Precautions
All products in the AAA Biotech catalog are strictly for research-use only, and are absolutely not suitable for use in any sort of medical, therapeutic, prophylactic, in-vivo, or diagnostic capacity. By purchasing a product from AAA Biotech, you are explicitly certifying that said products will be properly tested and used in line with industry standard. AAA Biotech and its authorized distribution partners reserve the right to refuse to fulfill any order if we have any indication that a purchaser may be intending to use a product outside of our accepted criteria.Disclaimer
Though we do strive to guarantee the information represented in this datasheet, AAA Biotech cannot be held responsible for any oversights or imprecisions. AAA Biotech reserves the right to adjust any aspect of this datasheet at any time and without notice. It is the responsibility of the customer to inform AAA Biotech of any product performance issues observed or experienced within 30 days of receipt of said product. To see additional details on this or any of our other policies, please see our Terms & Conditions page.Item has been added to Shopping Cart
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