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(A) Immunoblot analysis of BON-1 and QGP-1 cells treated with the DNMT inhibitor, Decitabine (400 nM for 72-hrs) shows increased expression of total <t>SSTR2</t> protein. (B) Immunoblot analysis confirms stable knockdown of DNMTs in BON-1 cells using pre-validated shRNA targeting DNMT1, DNMT3A and DNMT3B. Specific percent stable knockdown of each DNMT is noted (similar knockdown results in QGP-1 cells). (C) Immunoblot analysis reveals that stable knockdown of DNMT3B in both BON-1 and QGP-1 cells selectively increases expression of total SSTR2 protein. (D) Schematic of the human SSTR2 gene promoter element and CpG sites (red lines) having significantly decreased methylation levels (P < 0.05, at the least) after stable knockdown of DNMT3B in BON-1 and QGP-1 cells, compared to cells expressing control non-targeting shRNA (n=3). (E) Total protein levels in BON-1, QGP-1 and NT-3 cells correlates with SSTR2 gene promoter CpG methylation levels (n=3).

Sstr2, supplied by Boster Bio, used in various techniques. Bioz Stars score: 92/100, based on 5 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/sstr2/product/Boster Bio
Average 92 stars, based on 5 article reviews

sstr2 - by Bioz Stars, 2026-03

92/100 stars

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1) Product Images from "Multiple Epigenetic Mechanisms Functionally Cooperate to Silence Expression of Somatostatin Receptor Type 2 in Pancreatic Neuroendocrine Tumors"

Article Title: Multiple Epigenetic Mechanisms Functionally Cooperate to Silence Expression of Somatostatin Receptor Type 2 in Pancreatic Neuroendocrine Tumors

Journal: bioRxiv

doi: 10.1101/2025.09.23.677935

(A) Immunoblot analysis of BON-1 and QGP-1 cells treated with the DNMT inhibitor, Decitabine (400 nM for 72-hrs) shows increased expression of total SSTR2 protein. (B) Immunoblot analysis confirms stable knockdown of DNMTs in BON-1 cells using pre-validated shRNA targeting DNMT1, DNMT3A and DNMT3B. Specific percent stable knockdown of each DNMT is noted (similar knockdown results in QGP-1 cells). (C) Immunoblot analysis reveals that stable knockdown of DNMT3B in both BON-1 and QGP-1 cells selectively increases expression of total SSTR2 protein. (D) Schematic of the human SSTR2 gene promoter element and CpG sites (red lines) having significantly decreased methylation levels (P < 0.05, at the least) after stable knockdown of DNMT3B in BON-1 and QGP-1 cells, compared to cells expressing control non-targeting shRNA (n=3). (E) Total protein levels in BON-1, QGP-1 and NT-3 cells correlates with SSTR2 gene promoter CpG methylation levels (n=3).

Figure Legend Snippet: (A) Immunoblot analysis of BON-1 and QGP-1 cells treated with the DNMT inhibitor, Decitabine (400 nM for 72-hrs) shows increased expression of total SSTR2 protein. (B) Immunoblot analysis confirms stable knockdown of DNMTs in BON-1 cells using pre-validated shRNA targeting DNMT1, DNMT3A and DNMT3B. Specific percent stable knockdown of each DNMT is noted (similar knockdown results in QGP-1 cells). (C) Immunoblot analysis reveals that stable knockdown of DNMT3B in both BON-1 and QGP-1 cells selectively increases expression of total SSTR2 protein. (D) Schematic of the human SSTR2 gene promoter element and CpG sites (red lines) having significantly decreased methylation levels (P < 0.05, at the least) after stable knockdown of DNMT3B in BON-1 and QGP-1 cells, compared to cells expressing control non-targeting shRNA (n=3). (E) Total protein levels in BON-1, QGP-1 and NT-3 cells correlates with SSTR2 gene promoter CpG methylation levels (n=3).

Techniques Used: Western Blot, Expressing, Knockdown, shRNA, Methylation, Control, CpG Methylation Assay

(A) Immunoblot analysis demonstrates that stable knockdown of H3K9 histone methyltransferases, G9A and SETDB1, do not affect total SSTR2 protein expression. (B) Immunoblot analysis reveals that stable knockdown of the H3K27 histone methyltransferase, EZH2, increases expression of total SSTR2 protein in both BON-1 and QGP-1 cells. (C) Immunoblot analysis of both BON-1 and QGP-1 cells treated with the EZH2-specific inhibitor, Tazemetostat (1 uM for 96-hrs). Statistical analysis confirms significantly increased expression of SSTR2 protein expression after treatment with Tazemetostat. Data are expressed as mean ± SEM, **P < 0.01 (n=3). (D) Immunoblot analysis demonstrates that stable knockdown of RING2, a catalytic subunit of PRC1, increases expression of total SSTR2 protein.

Figure Legend Snippet: (A) Immunoblot analysis demonstrates that stable knockdown of H3K9 histone methyltransferases, G9A and SETDB1, do not affect total SSTR2 protein expression. (B) Immunoblot analysis reveals that stable knockdown of the H3K27 histone methyltransferase, EZH2, increases expression of total SSTR2 protein in both BON-1 and QGP-1 cells. (C) Immunoblot analysis of both BON-1 and QGP-1 cells treated with the EZH2-specific inhibitor, Tazemetostat (1 uM for 96-hrs). Statistical analysis confirms significantly increased expression of SSTR2 protein expression after treatment with Tazemetostat. Data are expressed as mean ± SEM, **P < 0.01 (n=3). (D) Immunoblot analysis demonstrates that stable knockdown of RING2, a catalytic subunit of PRC1, increases expression of total SSTR2 protein.

Techniques Used: Western Blot, Knockdown, Expressing

(A) Immunoblot analysis demonstrates that stable knockdown of the histone H3K4 lysine demethylases, JARID1A, increases expression of total SSTR2 protein in both BON-1 and QGP-1 cells. (B) Immunoblot analysis reveals that stable knockdown of LSD1, in both BON-1 and QGP-1 cells, increases expression of total SSTR2 protein. (C) Immunoblot analysis of both BON-1 and QGP-1 cells treated with the LSD1-specific inhibitor, ORY-1001 (1 uM for 72-hrs). Statistical analysis confirms significantly increased expression of SSTR2 protein after ORY-1001 treatment. Data are expressed as mean ± SEM, *P < 0.05 (n=3) (D) ChIP analysis demonstrates that treatment with ORY-1001 selectively increases activating marks, H3K4me1 and H3K27Ac, within the SSTR2 enhancer.

Figure Legend Snippet: (A) Immunoblot analysis demonstrates that stable knockdown of the histone H3K4 lysine demethylases, JARID1A, increases expression of total SSTR2 protein in both BON-1 and QGP-1 cells. (B) Immunoblot analysis reveals that stable knockdown of LSD1, in both BON-1 and QGP-1 cells, increases expression of total SSTR2 protein. (C) Immunoblot analysis of both BON-1 and QGP-1 cells treated with the LSD1-specific inhibitor, ORY-1001 (1 uM for 72-hrs). Statistical analysis confirms significantly increased expression of SSTR2 protein after ORY-1001 treatment. Data are expressed as mean ± SEM, *P < 0.05 (n=3) (D) ChIP analysis demonstrates that treatment with ORY-1001 selectively increases activating marks, H3K4me1 and H3K27Ac, within the SSTR2 enhancer.

Techniques Used: Western Blot, Knockdown, Expressing

(A) Immunoblot analysis demonstrates that stable knockdown of the CoREST subunit, RCOR1, in both BON-1 and QGP-1 cells does not affect total SSTR2 protein expression. (B) Immunoblot analysis reveals that stable knockdown of the essential NuRD complex factor, CHD4, increases total SSTR2 protein expression in both BON-1 and QGP-1 cells. (C) Immunoblot analysis shows that stable knockdown of the chromatin-remodeling protein, LSH, increases total SSTR2 protein in both BON-1 and QGP-1 cells.

Figure Legend Snippet: (A) Immunoblot analysis demonstrates that stable knockdown of the CoREST subunit, RCOR1, in both BON-1 and QGP-1 cells does not affect total SSTR2 protein expression. (B) Immunoblot analysis reveals that stable knockdown of the essential NuRD complex factor, CHD4, increases total SSTR2 protein expression in both BON-1 and QGP-1 cells. (C) Immunoblot analysis shows that stable knockdown of the chromatin-remodeling protein, LSH, increases total SSTR2 protein in both BON-1 and QGP-1 cells.

Techniques Used: Western Blot, Knockdown, Expressing

(A) Immunoblot analysis demonstrates that treatment with the HDACi, Entinostat (250 nM for 48-hrs), increases expression of total SSTR2-HiBiT protein and confirms that SSTR2-HiBiT expression is dynamically regulated by epigenetic-modifying compounds. (B) Quantitative high-throughput screening, using the MIPE 6.0 library, demonstrates 9 out of the top 10 top hits being members of the HDACi family. (C) Example combination drug screening of top hit drugs from primary screen. Rhomidepsin + Iadademstat and Panobinostat + Iadademstat. Readout is HiBiT luminescence.

Figure Legend Snippet: (A) Immunoblot analysis demonstrates that treatment with the HDACi, Entinostat (250 nM for 48-hrs), increases expression of total SSTR2-HiBiT protein and confirms that SSTR2-HiBiT expression is dynamically regulated by epigenetic-modifying compounds. (B) Quantitative high-throughput screening, using the MIPE 6.0 library, demonstrates 9 out of the top 10 top hits being members of the HDACi family. (C) Example combination drug screening of top hit drugs from primary screen. Rhomidepsin + Iadademstat and Panobinostat + Iadademstat. Readout is HiBiT luminescence.

Techniques Used: Western Blot, Expressing, High Throughput Screening Assay, Drug discovery

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Journal: bioRxiv

Article Title: Multiple Epigenetic Mechanisms Functionally Cooperate to Silence Expression of Somatostatin Receptor Type 2 in Pancreatic Neuroendocrine Tumors

doi: 10.1101/2025.09.23.677935

Figure Lengend Snippet: (A) Immunoblot analysis of BON-1 and QGP-1 cells treated with the DNMT inhibitor, Decitabine (400 nM for 72-hrs) shows increased expression of total SSTR2 protein. (B) Immunoblot analysis confirms stable knockdown of DNMTs in BON-1 cells using pre-validated shRNA targeting DNMT1, DNMT3A and DNMT3B. Specific percent stable knockdown of each DNMT is noted (similar knockdown results in QGP-1 cells). (C) Immunoblot analysis reveals that stable knockdown of DNMT3B in both BON-1 and QGP-1 cells selectively increases expression of total SSTR2 protein. (D) Schematic of the human SSTR2 gene promoter element and CpG sites (red lines) having significantly decreased methylation levels (P < 0.05, at the least) after stable knockdown of DNMT3B in BON-1 and QGP-1 cells, compared to cells expressing control non-targeting shRNA (n=3). (E) Total protein levels in BON-1, QGP-1 and NT-3 cells correlates with SSTR2 gene promoter CpG methylation levels (n=3).

Article Snippet: Primary antibodies utilized were: SSTR2 (BosterBio, M01689), DNMT1 (Epigentek, A-1700), DNMT3A (Santa Cruz Biotechnology, sc-365769), DNMT3B (Proteintech, 26971-1-AP), LSH/HELLS (Proteintech, 11955-1-AP) and HiBiT (Promega, N7200).

Techniques: Western Blot, Expressing, Knockdown, shRNA, Methylation, Control, CpG Methylation Assay

Journal: bioRxiv

Article Title: Multiple Epigenetic Mechanisms Functionally Cooperate to Silence Expression of Somatostatin Receptor Type 2 in Pancreatic Neuroendocrine Tumors

doi: 10.1101/2025.09.23.677935

Figure Lengend Snippet: (A) Immunoblot analysis demonstrates that stable knockdown of H3K9 histone methyltransferases, G9A and SETDB1, do not affect total SSTR2 protein expression. (B) Immunoblot analysis reveals that stable knockdown of the H3K27 histone methyltransferase, EZH2, increases expression of total SSTR2 protein in both BON-1 and QGP-1 cells. (C) Immunoblot analysis of both BON-1 and QGP-1 cells treated with the EZH2-specific inhibitor, Tazemetostat (1 uM for 96-hrs). Statistical analysis confirms significantly increased expression of SSTR2 protein expression after treatment with Tazemetostat. Data are expressed as mean ± SEM, **P < 0.01 (n=3). (D) Immunoblot analysis demonstrates that stable knockdown of RING2, a catalytic subunit of PRC1, increases expression of total SSTR2 protein.

Techniques: Western Blot, Knockdown, Expressing

Journal: bioRxiv

Article Title: Multiple Epigenetic Mechanisms Functionally Cooperate to Silence Expression of Somatostatin Receptor Type 2 in Pancreatic Neuroendocrine Tumors

doi: 10.1101/2025.09.23.677935

Figure Lengend Snippet: (A) Immunoblot analysis demonstrates that stable knockdown of the histone H3K4 lysine demethylases, JARID1A, increases expression of total SSTR2 protein in both BON-1 and QGP-1 cells. (B) Immunoblot analysis reveals that stable knockdown of LSD1, in both BON-1 and QGP-1 cells, increases expression of total SSTR2 protein. (C) Immunoblot analysis of both BON-1 and QGP-1 cells treated with the LSD1-specific inhibitor, ORY-1001 (1 uM for 72-hrs). Statistical analysis confirms significantly increased expression of SSTR2 protein after ORY-1001 treatment. Data are expressed as mean ± SEM, *P < 0.05 (n=3) (D) ChIP analysis demonstrates that treatment with ORY-1001 selectively increases activating marks, H3K4me1 and H3K27Ac, within the SSTR2 enhancer.

Techniques: Western Blot, Knockdown, Expressing

Journal: bioRxiv

Article Title: Multiple Epigenetic Mechanisms Functionally Cooperate to Silence Expression of Somatostatin Receptor Type 2 in Pancreatic Neuroendocrine Tumors

doi: 10.1101/2025.09.23.677935

Figure Lengend Snippet: (A) Immunoblot analysis demonstrates that stable knockdown of the CoREST subunit, RCOR1, in both BON-1 and QGP-1 cells does not affect total SSTR2 protein expression. (B) Immunoblot analysis reveals that stable knockdown of the essential NuRD complex factor, CHD4, increases total SSTR2 protein expression in both BON-1 and QGP-1 cells. (C) Immunoblot analysis shows that stable knockdown of the chromatin-remodeling protein, LSH, increases total SSTR2 protein in both BON-1 and QGP-1 cells.

Techniques: Western Blot, Knockdown, Expressing

Journal: bioRxiv

Article Title: Multiple Epigenetic Mechanisms Functionally Cooperate to Silence Expression of Somatostatin Receptor Type 2 in Pancreatic Neuroendocrine Tumors

doi: 10.1101/2025.09.23.677935

Figure Lengend Snippet: (A) Immunoblot analysis demonstrates that treatment with the HDACi, Entinostat (250 nM for 48-hrs), increases expression of total SSTR2-HiBiT protein and confirms that SSTR2-HiBiT expression is dynamically regulated by epigenetic-modifying compounds. (B) Quantitative high-throughput screening, using the MIPE 6.0 library, demonstrates 9 out of the top 10 top hits being members of the HDACi family. (C) Example combination drug screening of top hit drugs from primary screen. Rhomidepsin + Iadademstat and Panobinostat + Iadademstat. Readout is HiBiT luminescence.

Techniques: Western Blot, Expressing, High Throughput Screening Assay, Drug discovery

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1) Product Images from "Multiple Epigenetic Mechanisms Functionally Cooperate to Silence Expression of Somatostatin Receptor Type 2 in Pancreatic Neuroendocrine Tumors"

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