Review

shp77 (ATCC)

ATCC is a verified supplier

ATCC manufactures this product

About

News

Press Release

Team

Advisors

Partners

Contact

Bioz Stars

Bioz vStars

Buy from Supplier

Structured Review

ATCC shp77
Shp77, supplied by ATCC, used in various techniques. Bioz Stars score: 95/100, based on 137 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/shp77/SHP-77/pm41948931-213-11-30
Average 95 stars, based on 137 article reviews

shp77 - by Bioz Stars, 2026-10

95/100 stars

Images

Binding Assay:

Article Title: Multi-specific binding proteins for cancer treatment
Article Snippet: .. Interspecies cross-reactivity was determined by binding of DLL3/CD3 binding proteins to NCI-H82 (HTB-175TM) and SHP77 (ATCC®, CRL2195TM) cells, two SCLC cell lines, as well as to a recombinant cell line expressing cynomolgus DLL3 (generation of cell line described in Example 5). ..

Article Title: Multi-specific binding proteins for cancer treatment
Article Snippet: .. Binding of DLL3/CD3 binding proteins to human SCLC cell lines was tested by flow cytometry of NCI-H82 (HTB-175TM) and SHP77 (ATCC®, CRL-2195TM). ..

Recombinant:

Expressing:

Cell Culture:

Article Title: Multi-specific binding proteins for cancer treatment
Article Snippet: .. SCLC cell lines (FIG. 25A-F (in color): SHP77 (A and B), NCI-H82 (C and D), and NCI-H2286 (E and F) were cultured according to ATCC instructions with DLL3 #5 (FIGS. 25A, C, and E) or an isotype matched control (FIGS. 25B, D and F). .. Cells were scraped from the plate and fixed in Formalin and subsequently added to solubilized Histogel (Thermo Fisher scientific, HG-4000-012) and incubated over night at 4° C., followed by a standard paraffin embedding procedure performed in routine pathology laboratory.

Control:

other:

Article Title: Circular RMST cooperates with lineage-driving transcription factors to govern neuroendocrine transdifferentiation
Article Snippet: SHP77 , ATCC , CRL-2195.

Flow Cytometry:

Image Search Results

Figure 2. circRMST biogenesis is driven by conserved intronic repetitive element MIRb in humans and mice (A) Signal tracks of total RNA-seq in TKO GEMM and ENCODE mouse midbrain H3K4me3 ChIP-seq. Mouse transcript Rmst-207 (ENSMUST000000218678.3, GENCODE vM32) is shown. Curved lines above the TKO signal tracks indicate backsplicings with the thickest line indicating the most abundant isoform. Conservation score calculated by phyloP in 35 vertebrates is downloaded from UCSC genome browser. Human RMST-211 transcript is shown in reverse orientation. Red exons indicate the exons involved in circularization. Vertical gray lines represent short and long repetitive elements annotated in the human upstream intron. Red arrows represent MIRb elements. Schematic of CRISPR-dual guide designs to delete MIRbs is shown. (B) FPKM of circRmst isoforms identiﬁed in 4 SKO, 5 DKO and 4 TKO tumors. Wilcoxon rank-sum test. (C) Heatmap of 691 differential circRNAs (FDR <0.05) between 4 SKO and 4 TKO tumors calculated by the Wilcoxon rank-sum test. Color key indicates row Z score for each circRNA. (D) DNA gel electrophoresis of genomic PCR conﬁrming the human downstream MIRb deletion with guide set 2 in SHP77 single cell clones. WT, wild type. HOM, homozygous. Del, deletion. (E) circRMST expression by RT-qPCR. Expressions were normalized ﬁrst to GAPDH, then to wild-type clones. Unpaired two-tailed Student’s t test. (F) DNA gel electrophoresis of genomic PCR conﬁrming mouse downstream Mirb deletion at cell population level in KP1. (G) circRmst expression at cell population level by RT-qPCR. Expressions were ﬁrst normalized to Actb, then to cells with deletion of a gene desert region AAVS. Unpaired two-tailed Student’s t test. All error bars represent SD. *p < 0.05. **p < 0.01. ***p < 0.001. See also Figure S2 and Table S2.

Journal: Cancer cell

Article Title: Circular RMST cooperates with lineage-driving transcription factors to govern neuroendocrine transdifferentiation.

doi: 10.1016/j.ccell.2025.03.027

Figure Lengend Snippet: Figure 2. circRMST biogenesis is driven by conserved intronic repetitive element MIRb in humans and mice (A) Signal tracks of total RNA-seq in TKO GEMM and ENCODE mouse midbrain H3K4me3 ChIP-seq. Mouse transcript Rmst-207 (ENSMUST000000218678.3, GENCODE vM32) is shown. Curved lines above the TKO signal tracks indicate backsplicings with the thickest line indicating the most abundant isoform. Conservation score calculated by phyloP in 35 vertebrates is downloaded from UCSC genome browser. Human RMST-211 transcript is shown in reverse orientation. Red exons indicate the exons involved in circularization. Vertical gray lines represent short and long repetitive elements annotated in the human upstream intron. Red arrows represent MIRb elements. Schematic of CRISPR-dual guide designs to delete MIRbs is shown. (B) FPKM of circRmst isoforms identiﬁed in 4 SKO, 5 DKO and 4 TKO tumors. Wilcoxon rank-sum test. (C) Heatmap of 691 differential circRNAs (FDR <0.05) between 4 SKO and 4 TKO tumors calculated by the Wilcoxon rank-sum test. Color key indicates row Z score for each circRNA. (D) DNA gel electrophoresis of genomic PCR conﬁrming the human downstream MIRb deletion with guide set 2 in SHP77 single cell clones. WT, wild type. HOM, homozygous. Del, deletion. (E) circRMST expression by RT-qPCR. Expressions were normalized ﬁrst to GAPDH, then to wild-type clones. Unpaired two-tailed Student’s t test. (F) DNA gel electrophoresis of genomic PCR conﬁrming mouse downstream Mirb deletion at cell population level in KP1. (G) circRmst expression at cell population level by RT-qPCR. Expressions were ﬁrst normalized to Actb, then to cells with deletion of a gene desert region AAVS. Unpaired two-tailed Student’s t test. All error bars represent SD. *p < 0.05. **p < 0.01. ***p < 0.001. See also Figure S2 and Table S2.

Article Snippet: REAGENT or RESOURCE SOURCE IDENTIFIER ThruPLEX DNA-seq kit Takara cat. #R400677 SMARTer DNA Unique Dual Index Kit - 24U Set B Takara cat. #R400666 BioAnalyzer 2100 with Agilent high sensitivity DNA kit Agilent cat. #5067-4626 Deposited data SHP77 circRMST shRNA RNA-seq This study GEO GSE239702 SHP77 NKX2-1 siRNA RNA-seq This study GEO GSE239702 SHP77 SOX2 siRNA RNA-seq This study GEO GSE239702 SHP77 SOX2 ChIP-seq This study GEO GSE239702 SHP77 NKX2-1 ChIP-seq This study GEO GSE239702 CRPC NEPC total RNA-seq This study EGAS50000000897 Experimental models: Cell lines NCI-H889 Gift from Dr. Charles Rudin NCI-H1092 Gift from Dr. Charles Rudin NCI-H196 Gift from Dr. Charles Rudin NCI-H526 Gift from Dr. Kazukiro Yasufuku NCI-H82 Gift from Dr. Kazukiro Yasufuku 42F Gift from Dr. Amina Zoubeidi 293FT Thermofisher cat. #R70007 PM154 Puca et al., 2018 PM155 Puca et al., 2018 LTL331R This study KP1 Gift from Dr. Julien Sage SHP77 ATCC CRL-2195

Techniques: RNA Sequencing, ChIP-sequencing, CRISPR, DNA Gel Electrophoresis, Clone Assay, Expressing, Quantitative RT-PCR, Two Tailed Test

Figure 3. circRMST is essential for NE tumor growth and maintaining NE gene expressions including ASCL1 (A) Schematic of circRMST shRNA design. shRNA knockdown efﬁciency determined by divergent primers in SHP77 after 3 days of puromycin selection. Relative expression was ﬁrst normalized to GAPDH, then to shGFP. Unpaired two-tailed Student’s t-test. (B) Representative images of SCLC-A SHP77, H889, and H69 cell lines and NEPC organoid PM155, PM154, and PDX-derived 331R cell line grown in Matrigel after circRMST shRNA treatments. Cells were selected with puromycin for at least 3 days before seeding. Images were taken after 7 days to one month of cell growth. (C) Quantiﬁcation of colony numbers or organoid diameters. Two biological replicates were quantiﬁed. Relative colony numbers were normalized to shGFP. Unpaired two-tailed Student’s t test. (D) In vivo growth curves of SHP77 shRNA xenograft tumors (n = 7 for each group) in NSG mice. Error bars represent SEM. Two-way ANOVA. (E) Volcano plot showcasing RNA-seq gene expression changes in SHP77 treated with circRMST shRNA 1 compared to shGFP. Signiﬁcance and fold change were calculated with DESeq2. (F) Lollipop graph of all upregulated GSEA pathways and a selected subset of downregulated pathways in SHP77 circRMST shRNA cells compared to shGFP. Signiﬁcance is -log10(FDR). (G) Western blots of ASCL1 after circRMST knockdowns. (H) Schematic of RMST promoter deletion designs using CRISPR-dual guide system. (I) circRMST expression by RT-qPCR in SHP77 with DRMST promoter deletions at cell population level. Relative expression was ﬁrst normalized to GAPDH, then to DAAVS. Unpaired two-tailed Student’s t test. (legend continued on next page)

Journal: Cancer cell

Article Title: Circular RMST cooperates with lineage-driving transcription factors to govern neuroendocrine transdifferentiation.

doi: 10.1016/j.ccell.2025.03.027

Figure Lengend Snippet: Figure 3. circRMST is essential for NE tumor growth and maintaining NE gene expressions including ASCL1 (A) Schematic of circRMST shRNA design. shRNA knockdown efﬁciency determined by divergent primers in SHP77 after 3 days of puromycin selection. Relative expression was ﬁrst normalized to GAPDH, then to shGFP. Unpaired two-tailed Student’s t-test. (B) Representative images of SCLC-A SHP77, H889, and H69 cell lines and NEPC organoid PM155, PM154, and PDX-derived 331R cell line grown in Matrigel after circRMST shRNA treatments. Cells were selected with puromycin for at least 3 days before seeding. Images were taken after 7 days to one month of cell growth. (C) Quantiﬁcation of colony numbers or organoid diameters. Two biological replicates were quantiﬁed. Relative colony numbers were normalized to shGFP. Unpaired two-tailed Student’s t test. (D) In vivo growth curves of SHP77 shRNA xenograft tumors (n = 7 for each group) in NSG mice. Error bars represent SEM. Two-way ANOVA. (E) Volcano plot showcasing RNA-seq gene expression changes in SHP77 treated with circRMST shRNA 1 compared to shGFP. Signiﬁcance and fold change were calculated with DESeq2. (F) Lollipop graph of all upregulated GSEA pathways and a selected subset of downregulated pathways in SHP77 circRMST shRNA cells compared to shGFP. Signiﬁcance is -log10(FDR). (G) Western blots of ASCL1 after circRMST knockdowns. (H) Schematic of RMST promoter deletion designs using CRISPR-dual guide system. (I) circRMST expression by RT-qPCR in SHP77 with DRMST promoter deletions at cell population level. Relative expression was ﬁrst normalized to GAPDH, then to DAAVS. Unpaired two-tailed Student’s t test. (legend continued on next page)

Techniques: shRNA, Knockdown, Selection, Expressing, Two Tailed Test, Derivative Assay, In Vivo, RNA Sequencing, Gene Expression, Western Blot, CRISPR, Quantitative RT-PCR

$Figure 5. circRMST interacts with SOX2 and NKX2-1 (A) Schematic of circRMST pulldown assays with 30 biotin labeled DNA probes. (B and C) circRMST pulldown efﬁciency in SHP77 and H1092. Percentage of input was calculated comparing the pull-down fraction to the input. Unpaired two- tailed Student’s t test. (D) Cytoscape illustration of circRMST protein interactors identiﬁed in both SHP77 and H1092 in two biological replicates. SAINT analysis was applied comparing circRMST pulldowns and control pulldowns. All proteins had FDR <0.1. (E) Western blot of circRMST interacting and non-interacting proteins in SHP77 and H1092. (F) Enrichment of SOX2 and NKX2-1 with 1% formaldehyde crosslinked RIP in H889. IgG antibody was used as a negative control. (G) RNA enriched by SOX2 and NKX2-1 crosslinked RIP in H889. Percentage of input was calculated by comparing the IP fraction to the input. All error bars represent SD. **p < 0.01. See also Figure S5 and Table S4.$

Journal: Cancer cell

Article Title: Circular RMST cooperates with lineage-driving transcription factors to govern neuroendocrine transdifferentiation.

doi: 10.1016/j.ccell.2025.03.027

Figure Lengend Snippet: Figure 5. circRMST interacts with SOX2 and NKX2-1 (A) Schematic of circRMST pulldown assays with 30 biotin labeled DNA probes. (B and C) circRMST pulldown efﬁciency in SHP77 and H1092. Percentage of input was calculated comparing the pull-down fraction to the input. Unpaired two- tailed Student’s t test. (D) Cytoscape illustration of circRMST protein interactors identiﬁed in both SHP77 and H1092 in two biological replicates. SAINT analysis was applied comparing circRMST pulldowns and control pulldowns. All proteins had FDR <0.1. (E) Western blot of circRMST interacting and non-interacting proteins in SHP77 and H1092. (F) Enrichment of SOX2 and NKX2-1 with 1% formaldehyde crosslinked RIP in H889. IgG antibody was used as a negative control. (G) RNA enriched by SOX2 and NKX2-1 crosslinked RIP in H889. Percentage of input was calculated by comparing the IP fraction to the input. All error bars represent SD. **p < 0.01. See also Figure S5 and Table S4.

Techniques: Labeling, Two Tailed Test, Control, Western Blot, Negative Control

Figure 6. circRMST regulates NKX2-1 protein stability and SOX2 genomic binding (A) Western blot of NKX2-1 and SOX2 in SHP77 after 7 days of circRMST shRNA knockdown. SOX2 western was performed in the same experiment as ASCL1 shown in Figure 3G, and the Vinculin blot in Figure 3G serves as the loading control. (B) NKX2-1 protein amounts in 50 mg/mL cycloheximide (CHX) treated SHP77 with and without circRMST knockdown. Relative amounts from two biological replicates were normalized to vinculin and then to time point 0. Paired Student t tests. Error bars represent SD. (C) NKX2-1 protein amounts in SHP77 treated with baﬁlomycin A1 (BafA) at 200 nM for 24 h after 48 h of circRMST shRNA treatment. Band intensity was quantiﬁed by ImageJ, shown below NKX2-1 blots. LC3 was used as a positive control for BafA treatment. (D) Representative images of SHP77 live cells stained with 50 nM Deep Red LysoTracker for 1.5 h (E) Quantiﬁcation of LysoTracker signal intensity per cell using ImageJ. At least 5 images for each group were quantiﬁed. Unpaired two-tailed Student’s t test. (F) Western blot of NKX2-1 with circRMST and HSC70 shRNAs in SHP77. Band intensity was quantiﬁed by ImageJ, shown below NKX2-1 blots. (G) Proﬁle plots of SOX2 and NKX2-1 ChIP-seq signals at all peaks called by MACS2 in SHP77 with and without circRMST knockdown. (H) Heatmaps of SOX2 unaltered, downregulated and upregulated peaks in SHP77 circRMST knockdown cells, ﬁltered by FDR < 0.01 and fold change > 2. (I) ChIP-seq signal tracks for SOX2 and NKX2-1 at ASCL1 and INSM1 with and without circRMST knockdown. Yellow region represents signiﬁcantly differential peaks determined by DiffBind with p value < 0.05. (J) Western blots of CRISPR-Cas9 targeting SOX2 and/or NKX2-1 in SHP77. (K) Overlaps between SOX2 and NKX2-1 cistromes in SHP77. (L) Graphical summary of circRMST function in neuroendocrine tumors. *p < 0.05. **p < 0.01. ***p < 0.001. See also Figure S6 and Table S5.

Journal: Cancer cell

Article Title: Circular RMST cooperates with lineage-driving transcription factors to govern neuroendocrine transdifferentiation.

doi: 10.1016/j.ccell.2025.03.027

Figure Lengend Snippet: Figure 6. circRMST regulates NKX2-1 protein stability and SOX2 genomic binding (A) Western blot of NKX2-1 and SOX2 in SHP77 after 7 days of circRMST shRNA knockdown. SOX2 western was performed in the same experiment as ASCL1 shown in Figure 3G, and the Vinculin blot in Figure 3G serves as the loading control. (B) NKX2-1 protein amounts in 50 mg/mL cycloheximide (CHX) treated SHP77 with and without circRMST knockdown. Relative amounts from two biological replicates were normalized to vinculin and then to time point 0. Paired Student t tests. Error bars represent SD. (C) NKX2-1 protein amounts in SHP77 treated with baﬁlomycin A1 (BafA) at 200 nM for 24 h after 48 h of circRMST shRNA treatment. Band intensity was quantiﬁed by ImageJ, shown below NKX2-1 blots. LC3 was used as a positive control for BafA treatment. (D) Representative images of SHP77 live cells stained with 50 nM Deep Red LysoTracker for 1.5 h (E) Quantiﬁcation of LysoTracker signal intensity per cell using ImageJ. At least 5 images for each group were quantiﬁed. Unpaired two-tailed Student’s t test. (F) Western blot of NKX2-1 with circRMST and HSC70 shRNAs in SHP77. Band intensity was quantiﬁed by ImageJ, shown below NKX2-1 blots. (G) Proﬁle plots of SOX2 and NKX2-1 ChIP-seq signals at all peaks called by MACS2 in SHP77 with and without circRMST knockdown. (H) Heatmaps of SOX2 unaltered, downregulated and upregulated peaks in SHP77 circRMST knockdown cells, ﬁltered by FDR < 0.01 and fold change > 2. (I) ChIP-seq signal tracks for SOX2 and NKX2-1 at ASCL1 and INSM1 with and without circRMST knockdown. Yellow region represents signiﬁcantly differential peaks determined by DiffBind with p value < 0.05. (J) Western blots of CRISPR-Cas9 targeting SOX2 and/or NKX2-1 in SHP77. (K) Overlaps between SOX2 and NKX2-1 cistromes in SHP77. (L) Graphical summary of circRMST function in neuroendocrine tumors. *p < 0.05. **p < 0.01. ***p < 0.001. See also Figure S6 and Table S5.

Techniques: Binding Assay, Western Blot, shRNA, Knockdown, Control, Positive Control, Staining, Two Tailed Test, ChIP-sequencing, CRISPR

Review

shp77 (ATCC)

Structured Review

Images

Related Articles

Binding Assay:

Recombinant:

Expressing:

Cell Culture:

Control:

other:

Flow Cytometry:

Similar Products

Image Search Results