BMS144
antibody from Invitrogen Antibodies
Targeting: CD44
CD44R, CSPG8, HCELL, IN, MC56, MDU2, MDU3, MIC4, Pgp1
Antibody data
- Antibody Data
- Antigen structure
- References [4]
- Comments [0]
- Validations
- Other assay [4]
Submit
Validation data
Reference
Comment
Report error
- Product number
- BMS144 - Provider product page
- Provider
- Invitrogen Antibodies
- Product name
- CD44var (v3) Monoclonal Antibody (VFF-327v3), eBioscience™
- Antibody type
- Monoclonal
- Antigen
- Other
- Description
- Description: Specifically recognizes an epitope encoded by exon v3 on the variant portion of human CD44. Standard CD44 (CD44s) lacks the entire variable region and is found mainly in cells of lymphohematopoietic origin. The multiple isoforms (designated CD44v; v = variant) contain alternatively spliced exons inserted within the extracellular domain. These isoforms are known as CD44v1, CD44v2, CD44v3, CD44v4, CD44v5, CD44v6, CD44v7, CD44v8, CD44v9, CD44v10, CD44v11. Applications Tested: Flow Cytometry, Immunohistochemistry (Paraffin), Western Blotting.
- Reactivity
- Human
- Host
- Mouse
- Isotype
- IgG
- Antibody clone number
- VFF-327v3
- Vial size
- 100 µg
- Concentration
- 1 mg/mL
- Storage
- -20°C
Submitted references The COOH-Terminal Proline-Rich Region of GRP78 Is a Key Regulator of Its Cell Surface Expression and Viability of Tamoxifen-Resistant Breast Cancer Cells.
GRP78 regulates CD44v membrane homeostasis and cell spreading in tamoxifen-resistant breast cancer.
Senescent Atrophic Epidermis Retains Lrig1+ Stem Cells and Loses Wnt Signaling, a Phenotype Shared with CD44KO Mice.
Lrig1 Expression in Human Sebaceous Gland Tumors.
Tseng CC, Zhang P, Lee AS
Neoplasia (New York, N.Y.) 2019 Aug;21(8):837-848
Neoplasia (New York, N.Y.) 2019 Aug;21(8):837-848
GRP78 regulates CD44v membrane homeostasis and cell spreading in tamoxifen-resistant breast cancer.
Tseng CC, Stanciauskas R, Zhang P, Woo D, Wu K, Kelly K, Gill PS, Yu M, Pinaud F, Lee AS
Life science alliance 2019 Aug;2(4)
Life science alliance 2019 Aug;2(4)
Senescent Atrophic Epidermis Retains Lrig1+ Stem Cells and Loses Wnt Signaling, a Phenotype Shared with CD44KO Mice.
Barnes L, Saurat JH, Kaya G
PloS one 2017;12(1):e0169452
PloS one 2017;12(1):e0169452
Lrig1 Expression in Human Sebaceous Gland Tumors.
Pünchera J, Barnes L, Kaya G
Dermatopathology (Basel, Switzerland) 2016 Apr-Jun;3(2):44-54
Dermatopathology (Basel, Switzerland) 2016 Apr-Jun;3(2):44-54
No comments: Submit comment
Supportive validation
- Submitted by
- Invitrogen Antibodies (provider)
- Main image
- Experimental details
- Figure 4. Knockdown of GRP78 or CD44 alters cell morphology, reduces cell attachment, and impedes cell spreading in MCF7-LR cells. (A) Left: Western blot analysis of WCLs prepared from MCF7-LR cells transfected with control siRNA (sictrl) or siRNAs targeting GRP78 coding sequence, si78(1), or 3' untranslated region (3'-UTR), si78(2), using antibodies against GRP78 (MAb159) or HSP70 (C92F3A-5). GAPDH served as a loading control. Right: Quantification of relative levels of GRP78 and HSP70. Data represents mean +- SEM from three biological repeats. (B) Sequence comparison of GRP78 siRNA target sites on human GRP78 and HSP70 genes. (C) Bright-field micrographs showing the morphology of MCF7-LR cells transfected with sictrl or siRNA targeting GRP78 or CD44 . siCD44(1) targets 3'-UTR and siCD44(2) targets the common coding sequence. Scale bar, 100 mum. (D) Epifluorescent micrographs showing the F-actin organization of MCF7-LR cells transfected with sictrl or siRNA targeting GRP78 or CD44 . The arrows indicate the F-actin bundles. Red, F-actin labeled with rhodamine phalloidin; blue, nuclei stained by DAPI. Scale bar, 50 mum. (E) Cell attachment assay. MCF7-LR cells were transfected with sictrl or siRNA targeting GRP78 or CD44 for 60 h before re-seeding onto collagen I-coated culture plates for 1 h. Attached cells were visualized by crystal violet staining. Scale bar, 50 mum. (F) Quantification of relative levels of cell attachment described in panel (E). Crystal violet staining o
- Submitted by
- Invitrogen Antibodies (provider)
- Main image
- Experimental details
- Figure S3. Knockdown efficiency of siRNAs against CD44 in MCF7-LR cells. (A) Epifluorescent micrographs showing the levels of CD44 in MCF7-LR cells transfected with control siRNA (sictrl) or siRNAs targeting CD44 for 60 h. Cells were permeabilized by Triton X-100 and immunostained with the anti-CD44 antibody against a common epitope of CD44 isoforms (green, 15675-1-AP) or specifically the v3 exon (red, BMS144). No primary control staining lacked the primary antibody. The images were acquired by Keyence microscope (BM-X710) with a 20x objective. Nuclei were stained by DAPI in blue. Scale bars, 50 mum. (B) Quantification of relative levels of CD44. Number of analyzed independent image areas (A) and cells (N): A/N = 4/1,322, sictrl; 5/1,059, siCD44(1); 5/707, siCD44(2). Data represent mean +- SEM. ** P < 0.01, *** P < 0.001 ( t test).
- Submitted by
- Invitrogen Antibodies (provider)
- Main image
- Experimental details
- Figure 1 GRP78 colocalizes with CD44v in MCF7-LR breast cancer cells. (A) Immunofluorescence and confocal images showing the distribution and colocalization of GRP78 (red) and CD44v (green) in the saponin-permeabilized MCF7-LR breast cancer cells. GRP78 and CD44v were detected by MAb159 and anti-CD44v3 antibodies, respectively. The mouse-on-mouse (M.O.M.) control staining was performed with the same protocol as double-stained cells but lacking the primary antibody targeting CD44v. No primary control staining was conducted without the primary antibodies but with secondary antibodies. The nuclei were stained by DAPI in blue. Thickness of single immunofluorescent image section: 0.3 mum. Signals were visualized with 63x/1.4 NA objective on a Leica TCS SP8 confocal microscope. Scale bars, 20 mum. (B) Immunofluorescence and confocal images showing the distribution and colocalization of GRP78 (red) and CD44v (green) on the cell surface of nonpermeabilized MCF7-LR breast cancer cells. GRP78 and CD44v were detected by MAb159 and anti-CD44v3 antibodies, respectively. The M.O.M. control staining was performed with the same protocol as double-stained cells but lacking primary antibody targeting CD44v. No primary control staining was conducted without the primary antibodies but with secondary antibodies. The nuclei were stained by DAPI in blue. DIC: differential interference contrast. Thickness of single immunofluorescent image section: 0.8 mum. Cell peripheries were outlined with black l
- Submitted by
- Invitrogen Antibodies (provider)
- Main image
- Experimental details
- Figure 5 Enforced expression of short peptide encoding the proline-rich region of GRP78 reduced cell viability and promoted apoptosis in MCF7-LR breast cancer cells. (A) Schematic illustration of expression plasmids containing wild-type or mutant sequences encoding 20 amino acids spanning the proline-rich region of GRP78 (a.a. 640-642). The sequences were preceded by a secretory and sorting peptide sequence of alpha-melanocyte-stimulating hormone (SSP). The plasmids were constructed in pcDNA3 backbone vector (v). P, the plasmid containing wild-type proline-rich sequence. mP, the plasmid containing PPP to AAA mutation. (B) Schematic representation of experimental procedures. cM, conditional media. h, hours. (C) Bright-field images of MCF7-LR cells with the enforced expression of v, P, or mP. Images were photographed 48 hours post transfection. Scale bar, 50 mum. (D) Left: Western blot analysis of whole cell lysates from MCF7-LR cells transfected with v, P, or mP. Cells lysates were collected 48 hours posttransfection. CD44v and GRP78 were detected by anti-CD44v3 and MAb159 antibodies, respectively. beta-Actin is loading control. Right: Quantification of CD44v levels compared to the control. Data represent means +- SEM from three biological repeats. * P