Anti-YAP1 (phospho Y357) antibody

• WB

Unknown

Western blot - Anti-YAP1 (phospho Y357) antibody (AB62751)

All lanes:

Western blot - Anti-YAP1 (phospho Y357) antibody (ab62751) at 1/2000 dilution

Lane 1:

Whole cell lysates of HEK-293T cells co-transfected with human YAP1 and human c-Abl

Lane 2:

Whole cell lysates of untransfected HEK-293T cells

Lane 3:

Whole cell lysates of HEK-293T cells co-transfected with human YAP1 and human c-Abl with YAP1 peptide (human 351-362)

Lane 4:

Whole cell lysates of HEK-293T cells co-transfected with human YAP1 and human c-Abl with phospho-YAP1 (human 351-362 [phospho Y357]) immunizing peptide

Secondary

All lanes:

Goat Anti-Rabbit IgG, Peroxidase conjugate

Predicted band size: 54 kDa

Observed band size: 100 kDa,65 kDa,70 kDa

false

• WB

CiteAb

Western blot - Anti-YAP1 (phospho Y357) antibody (AB62751)

Western Blotting using Anti-YAP1 (phospho Y357) antibody, ab62751. Publication image from Han, T. et al., 2019, Nat Commun, 31420536. Legend direct from paper.

Cdh1 negatively regulates Src kinase activity in an APC-independent manner. a–c Immunoblot (IB) analysis of MCF7 (a), MDA-MB-231 (b), and BT474 (c) cells infected with control (shScramble, shScr for short) or the indicated shCdh1 lentiviral shRNA constructs. The infected cells were selected with 1 µg ml−1 puromycin for 72 h before harvest. d CRISPR/Cas9-mediated deletion of Cdh1 activated Src. IB analysis of MCF7 cells infected with control (sgGFP) or sgCdh1 lentiviral construct. The infected cells were selected with 1 µg ml−1 puromycin for 7 days before plating for single clone selection. e Src was activated in Cdh1−/− MEFs. IB analysis of WT and Cdh1−/− MEFs treated with 4 ng ml−1 PDGF for the indicated periods of time after 16 h serum deprivation. f IB analysis of MCF7 cells infected with the indicated lentiviral shRNA constructs. The infected cells were selected with 1 µg ml−1 puromycin for 72 h before harvest. g, h IB analysis of MCF7 cells infected with control (shScr) or the indicated shCdc27 (g) and shAPC10 (h) lentiviral shRNA constructs. The infected cells were selected with 1 µg ml−1 puromycin for 72 h before harvest. i MCF7 cells stably expressing retroviral empty vector (EV), WT-, or N-Cdh1 were further infected with shScr or shCdh1 lentiviral constructs as indicated. The infected cells were selected with 1 µg ml−1 puromycin for 72 h before harvest. *Cdh1 cDNA used in this experiment has been mutated to escape shCdh1-mediated gene silencing. ** indicates nonspecific bands. j IB analysis of T47D cells infected with the indicated lentiviral shRNA constructs. The infected cells were selected with 1 µg ml−1 puromycin and 100 µg ml−1 hygromycin for 72 h before harvest. k IB analysis of WCL derived from sgGFP- and sgCdh1-infected MDA-MB-231 cells that were synchronized at the G1–S boundary by double-thymidine block and then released back into the cell cycle for the indicated periods of time

false

• WB

CiteAb

Western blot - Anti-YAP1 (phospho Y357) antibody (AB62751)

Western Blotting using Anti-YAP1 (phospho Y357) antibody, ab62751. Publication image from Han, T. et al., 2019, Nat Commun, 31420536. Legend direct from paper.

Cdh1 negatively regulates Src kinase activity in an APC-independent manner. a–c Immunoblot (IB) analysis of MCF7 (a), MDA-MB-231 (b), and BT474 (c) cells infected with control (shScramble, shScr for short) or the indicated shCdh1 lentiviral shRNA constructs. The infected cells were selected with 1 µg ml−1 puromycin for 72 h before harvest. d CRISPR/Cas9-mediated deletion of Cdh1 activated Src. IB analysis of MCF7 cells infected with control (sgGFP) or sgCdh1 lentiviral construct. The infected cells were selected with 1 µg ml−1 puromycin for 7 days before plating for single clone selection. e Src was activated in Cdh1−/− MEFs. IB analysis of WT and Cdh1−/− MEFs treated with 4 ng ml−1 PDGF for the indicated periods of time after 16 h serum deprivation. f IB analysis of MCF7 cells infected with the indicated lentiviral shRNA constructs. The infected cells were selected with 1 µg ml−1 puromycin for 72 h before harvest. g, h IB analysis of MCF7 cells infected with control (shScr) or the indicated shCdc27 (g) and shAPC10 (h) lentiviral shRNA constructs. The infected cells were selected with 1 µg ml−1 puromycin for 72 h before harvest. i MCF7 cells stably expressing retroviral empty vector (EV), WT-, or N-Cdh1 were further infected with shScr or shCdh1 lentiviral constructs as indicated. The infected cells were selected with 1 µg ml−1 puromycin for 72 h before harvest. *Cdh1 cDNA used in this experiment has been mutated to escape shCdh1-mediated gene silencing. ** indicates nonspecific bands. j IB analysis of T47D cells infected with the indicated lentiviral shRNA constructs. The infected cells were selected with 1 µg ml−1 puromycin and 100 µg ml−1 hygromycin for 72 h before harvest. k IB analysis of WCL derived from sgGFP- and sgCdh1-infected MDA-MB-231 cells that were synchronized at the G1–S boundary by double-thymidine block and then released back into the cell cycle for the indicated periods of time

false

• WB

CiteAb

Western blot - Anti-YAP1 (phospho Y357) antibody (AB62751)

Western Blotting using Anti-YAP1 (phospho Y357) antibody, ab62751. Publication image from Han, T. et al., 2019, Nat Commun, 31420536. Legend direct from paper.

Cdh1 negatively regulates Src kinase activity in an APC-independent manner. a–c Immunoblot (IB) analysis of MCF7 (a), MDA-MB-231 (b), and BT474 (c) cells infected with control (shScramble, shScr for short) or the indicated shCdh1 lentiviral shRNA constructs. The infected cells were selected with 1 µg ml−1 puromycin for 72 h before harvest. d CRISPR/Cas9-mediated deletion of Cdh1 activated Src. IB analysis of MCF7 cells infected with control (sgGFP) or sgCdh1 lentiviral construct. The infected cells were selected with 1 µg ml−1 puromycin for 7 days before plating for single clone selection. e Src was activated in Cdh1−/− MEFs. IB analysis of WT and Cdh1−/− MEFs treated with 4 ng ml−1 PDGF for the indicated periods of time after 16 h serum deprivation. f IB analysis of MCF7 cells infected with the indicated lentiviral shRNA constructs. The infected cells were selected with 1 µg ml−1 puromycin for 72 h before harvest. g, h IB analysis of MCF7 cells infected with control (shScr) or the indicated shCdc27 (g) and shAPC10 (h) lentiviral shRNA constructs. The infected cells were selected with 1 µg ml−1 puromycin for 72 h before harvest. i MCF7 cells stably expressing retroviral empty vector (EV), WT-, or N-Cdh1 were further infected with shScr or shCdh1 lentiviral constructs as indicated. The infected cells were selected with 1 µg ml−1 puromycin for 72 h before harvest. *Cdh1 cDNA used in this experiment has been mutated to escape shCdh1-mediated gene silencing. ** indicates nonspecific bands. j IB analysis of T47D cells infected with the indicated lentiviral shRNA constructs. The infected cells were selected with 1 µg ml−1 puromycin and 100 µg ml−1 hygromycin for 72 h before harvest. k IB analysis of WCL derived from sgGFP- and sgCdh1-infected MDA-MB-231 cells that were synchronized at the G1–S boundary by double-thymidine block and then released back into the cell cycle for the indicated periods of time

false

• WB

CiteAb

Western blot - Anti-YAP1 (phospho Y357) antibody (AB62751)

Western Blotting using Anti-YAP1 (phospho Y357) antibody, ab62751. Publication image from Han, T. et al., 2019, Nat Commun, 31420536. Legend direct from paper.

Cdh1-binding deficient Src mutant promotes breast cancer cell growth. a Immunoblot (IB) analysis of whole-cell lysates (WCL) derived from MDA-MB-231 cells stably expressing empty vector (EV), WT-Src, D-box-1-mutated, or D-box-2-mutated Src. b MDA-MB-231 cells generated in (c) were subjected to cell proliferation assays in DMEM medium supplemented with 10% FBS for 6 days. Cell viability was determined at the indicated time points. The relative cell viability was calculated as mean ± SD (n = 3). *P < 0.05; Student’s t test. c, d MDA-MB-231 cells generated in (a) were seeded for clonogenic survival assays (1000 cells per well). Fourteen days after plating, crystal violet was used to stain the formed colonies (c) and the relative colony numbers were counted as mean ± SD (n = 3), *P < 0.05; Student’s t test (d). e, f MDA-MB-231 cells generated in (a) were subjected to soft agar colony formation assays for 21 days. Formed colonies were stained with iodonitrotetrazolium chloride (INT) (e). The relative colony numbers were calculated as mean ± SD (n = 3). *P < 0.05; Student’s t test (f). g, h MDA-MB-231 cells generated in (a) were subjected to Matrigel invasion assays for 24 h. Invaded cells were stained with phalloidin (g). The invaded distance was calculated as mean ± SD (n = 5). *P < 0.05; Student’s t test (h). i, j MDA-MB-231 cells generated in Supplementary Fig. 5g were seeded for clonogenic survival assays (1000 cells per well). Fourteen days after plating, crystal violet was used to stain the formed colonies (i) and the relative colony numbers were counted as mean ± SD (n = 3), *P < 0.05; Student’s t test (j). k, l Tumor pictures (k) and the growth curves (l) for the xenograft experiments with the MDA-MB-231 cells generated in (a) were inoculated subcutaneously. In each flank of the nude mice, 1 x 106 cells were injected. The visible tumors were measured at the indicated days. Error bars represent ±SEM (n = 4). *P < 0.05; Student’s t test

false