lsd1 (Bethyl)

Bethyl lsd1

Lsd1, supplied by Bethyl, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/lsd1+function/BHC110%2FLSD1+Antibody/pm30992567-356-7-8
Average 93 stars, based on 1 article reviews

lsd1 - by Bioz Stars, 2026-10

93/100 stars

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lsd1 (Guiyang Xintian Pharmaceutical Co Ltd)

Guiyang Xintian Pharmaceutical Co Ltd lsd1

Lsd1, supplied by Guiyang Xintian Pharmaceutical Co Ltd, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/lsd1+function/lsd1/10__1515_slash_oncologie___2023___0562-19-11-38
Average 86 stars, based on 1 article reviews

lsd1 - by Bioz Stars, 2026-10

86/100 stars

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primary antibodies for lsd1 (Novus Biologicals)

Novus Biologicals primary antibodies for lsd1

Confirmation of mRNA expression of AR, JMJD2A, <t>LSD1</t> in bladder cancer cell lines (A). Full length gels are presented in supplemental figure 1. The number of PCR cycles employed for each gene is indicated. GAPDH served as an internal control for cDNA integrity. Comparison of effects of 3mM and 1mM pargline and tranylcypromine (Tranyl) on proliferation of HTB-1 (B), HTB-5 (C), HTB-3 (D) and HT-1376 (E) bladder cancer cells. Quantitative RT-PCR was used to assess the effects of tranylcypromine on androgen regulated transcription (F). Neutral endopeptidase (NEP) is a representative AR-regulated gene expressed in both HTB1 and HTB5 bladder cancer cells. Bladder cells were treated with tranylcypromine (50µM) for 48 hours prior to transcriptional activation with the R1881 (1nM) synthetic androgen for 30 minutes. R1881 induces NEP expression in AR-positive HTB5 cells. This effect of R1881 on NEP expression in HTB5 cells is impaired by tranylcypromine. Neither R1881 nor tranylcypromine alter NEP expression in AR-negative HTB1 cells, suggesting the effects of tranylcypromine are dependent upon the presence of a functional AR-KDM complex.(*:p<0.05, ***p<0.01, ns: not significant).

Primary Antibodies For Lsd1, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/lsd1+function/LSD1+Antibody+(1B2E5)/pmc03315373-143-0-6
Average 94 stars, based on 1 article reviews

primary antibodies for lsd1 - by Bioz Stars, 2026-10

94/100 stars

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Image Search Results

Journal: Nature chemical biology

Article Title: CRISPR-suppressor scanning reveals a nonenzymatic role of LSD1 in AML.

doi: 10.1038/s41589-019-0263-0

Figure Lengend Snippet: Fig. 1 | CRISPR-suppressor scanning identifies regions of LSD1 that mediate its function and susceptibility to pharmacological inhibitors. a, Schematic of CRISPR-suppressor scanning workflow to profile SARs of LSD1 small-molecule inhibitors. b, Heat maps depicting log2(fold-change sgRNA enrichment) in SET-2 at the indicated time points and conditions versus week 0 normalized against functionally neutral genome-targeting control sgRNAs. The sgRNAs are arrayed on the x axis by the LSD1 CDS. Color represents mean values across three replicate transductions. c, Scatter plot showing log2(fold-change sgRNA enrichment) in SET-2 under GSK-LSD1 treatment at week 8 versus week 0 normalized against functionally neutral genome-targeting control sgRNAs. The sgRNAs are arrayed on the x axis by the LSD1 CDS. Data represent mean values across three replicate transductions. d, Heat map showing cross-correlation of overall sgRNA enrichment at the specified time points during the CRISPR-suppressor scanning in SET-2. Data represent mean values across three replicate transductions.

Article Snippet: The primary antibodies used are as follows: LSD1 (Bethyl Laboratories A300-215A, LOT number 2); GFI1B (B-7) X (Santa Cruz Biotechnology sc-28356X, LOT number D1615); monoclonal anti-FLAG M2 (Sigma-Aldrich F1804, LOT number SLBW3851); GAPDH (Santa Cruz Biotechnology sc-477724, LOT number B0210); and GFI1B (Santa Cruz Biotechnology sc-28356X, LOT number D1615).

Techniques: CRISPR, Control

Fig. 2 | Spatial clustering of CRISPR-suppressor scanning data reveals potential functional hotspots of LSD1 that mediate drug action. a,b, Heat maps depicting the PWES between sgRNAs ordered by the CDS (a) or by hierarchical clustering (b). sgRNAs targeting the disordered LSD1 N terminus were omitted in this analysis because this domain was truncated in structural studies. c, Box plot showing the enrichment of sgRNA groups as defined by hierarchical clustering in b for SET-2 under GSK-LSD1 treatment at week 8. The y axis represents mean log2(fold-change sgRNA enrichment) at week 8 versus week 0 across three replicate transductions. In the plot, bars represent the median, the box represents the interquartile range (IQR) and the whiskers represent 1.5 × IQR. d, Structural view of LSD1 complexed with a SNAG peptide (magenta) showing the location of clusters 1 (red) and 5 (blue) defined in b (Protein Data Bank (PDB): 2Y48).

Journal: Nature chemical biology

Article Title: CRISPR-suppressor scanning reveals a nonenzymatic role of LSD1 in AML.

doi: 10.1038/s41589-019-0263-0

Figure Lengend Snippet: Fig. 2 | Spatial clustering of CRISPR-suppressor scanning data reveals potential functional hotspots of LSD1 that mediate drug action. a,b, Heat maps depicting the PWES between sgRNAs ordered by the CDS (a) or by hierarchical clustering (b). sgRNAs targeting the disordered LSD1 N terminus were omitted in this analysis because this domain was truncated in structural studies. c, Box plot showing the enrichment of sgRNA groups as defined by hierarchical clustering in b for SET-2 under GSK-LSD1 treatment at week 8. The y axis represents mean log2(fold-change sgRNA enrichment) at week 8 versus week 0 across three replicate transductions. In the plot, bars represent the median, the box represents the interquartile range (IQR) and the whiskers represent 1.5 × IQR. d, Structural view of LSD1 complexed with a SNAG peptide (magenta) showing the location of clusters 1 (red) and 5 (blue) defined in b (Protein Data Bank (PDB): 2Y48).

Techniques: CRISPR, Functional Assay

Fig. 3 | CRISPR-suppressor scanning enables profiling of LSD1 SARs. a, Structures of LSD1 inhibitors used in CRISPR-suppressor scanning. For each compound, Ki and GI50 values were measured across three replicates, where Ki is the equilibrium dissociation constant and GI50 is the drug concentration that results in half-maximal inhibition of cell proliferation. See Supplementary Fig. 3a–c for further details. b, Heat maps showing sgRNA enrichment measured in SET-2 at week 6. The sgRNAs are arrayed on the x axis by the LSD1 CDS. Color represents mean log2(fold-change sgRNA enrichment normalized to vehicle treatment) across three replicate transductions. FC = fold-change. c, Scatter plot showing projection of compound sgRNA enrichment profiles at week 6 onto principal component space. Groups of compounds were identified by k-means clustering (k = 3) and are marked. Data represent mean values across three replicate transductions. d, Heat map showing sgRNA enrichment measured in SET-2 at week 6 for the top five sgRNAs with largest principal component coefficient loadings and bottom five sgRNAs with smallest principal component coefficient loadings. The sgRNAs are ordered on the x axis by principal component coefficient, increasing from left to right, and are labeled according to the residues they target in the LSD1 CDS. Color represents mean log2(fold-change) of sgRNA enrichment normalized to vehicle treatment across three replicate transductions. e, Left, heat map showing mutation enrichment in sequenced exons across different drug treatment conditions. Mutated reads are defined as any read containing a modification in a coding region. Color represents log2(fold-change mutated reads) of drug-treatment relative to vehicle treatment at week 6. DNA from three replicate transductions were pooled at equal concentrations before sequencing to obtain an average log2(fold-change) of mutated reads. Right, schematic shows the genotypes of the most abundant mutation in exon 15 for each treatment condition at week 6. Percentages indicate the allele frequency as determined through sequencing. Bottom, schematic depicts the LSD1 gene locus and the regions sequenced. f, Homology model of LSD1 (K661E) overlaid with wild-type LSD1 is shown. W695, involved in a hydrophobic interaction with GSK690, is rotated out of plane in the model of the mutant structure (PDB: 2HKO). g, Homology model of LSD1 L659_N660insK overlaid with wild-type LSD1 is shown. The N5 atom of FAD and K661 are involved in a water-mediated hydrogen-bonding network (PDB: 2HKO).

Journal: Nature chemical biology

Article Title: CRISPR-suppressor scanning reveals a nonenzymatic role of LSD1 in AML.

doi: 10.1038/s41589-019-0263-0

Figure Lengend Snippet: Fig. 3 | CRISPR-suppressor scanning enables profiling of LSD1 SARs. a, Structures of LSD1 inhibitors used in CRISPR-suppressor scanning. For each compound, Ki and GI50 values were measured across three replicates, where Ki is the equilibrium dissociation constant and GI50 is the drug concentration that results in half-maximal inhibition of cell proliferation. See Supplementary Fig. 3a–c for further details. b, Heat maps showing sgRNA enrichment measured in SET-2 at week 6. The sgRNAs are arrayed on the x axis by the LSD1 CDS. Color represents mean log2(fold-change sgRNA enrichment normalized to vehicle treatment) across three replicate transductions. FC = fold-change. c, Scatter plot showing projection of compound sgRNA enrichment profiles at week 6 onto principal component space. Groups of compounds were identified by k-means clustering (k = 3) and are marked. Data represent mean values across three replicate transductions. d, Heat map showing sgRNA enrichment measured in SET-2 at week 6 for the top five sgRNAs with largest principal component coefficient loadings and bottom five sgRNAs with smallest principal component coefficient loadings. The sgRNAs are ordered on the x axis by principal component coefficient, increasing from left to right, and are labeled according to the residues they target in the LSD1 CDS. Color represents mean log2(fold-change) of sgRNA enrichment normalized to vehicle treatment across three replicate transductions. e, Left, heat map showing mutation enrichment in sequenced exons across different drug treatment conditions. Mutated reads are defined as any read containing a modification in a coding region. Color represents log2(fold-change mutated reads) of drug-treatment relative to vehicle treatment at week 6. DNA from three replicate transductions were pooled at equal concentrations before sequencing to obtain an average log2(fold-change) of mutated reads. Right, schematic shows the genotypes of the most abundant mutation in exon 15 for each treatment condition at week 6. Percentages indicate the allele frequency as determined through sequencing. Bottom, schematic depicts the LSD1 gene locus and the regions sequenced. f, Homology model of LSD1 (K661E) overlaid with wild-type LSD1 is shown. W695, involved in a hydrophobic interaction with GSK690, is rotated out of plane in the model of the mutant structure (PDB: 2HKO). g, Homology model of LSD1 L659_N660insK overlaid with wild-type LSD1 is shown. The N5 atom of FAD and K661 are involved in a water-mediated hydrogen-bonding network (PDB: 2HKO).

Techniques: CRISPR, Concentration Assay, Inhibition, Labeling, Mutagenesis, Modification, Sequencing

Fig. 5 | An orthogonal drug-complementary GFI1B allele establishes sufficiency of the LSD1–GFI1B interaction for AML survival. a, Co-IP of wild-type FLAG–LSD1 and FLAG–LSD1 mutant variants with GFI1B was performed after vehicle or GSK-LSD1 treatment (250 nM, 48 h) in transiently transfected HEK 293T cells. Co-IP was performed using an anti-GFI1B antibody. LSD1 was detected using an anti-FLAG antibody. One of two independent replicates is shown. See Supplementary Fig. 7c for uncropped blot. b, Illustration depicting the concept of an orthogonal drug-complementary GFI1B allele that can only bind LSD1 in the presence of GSK-LSD1. c, Structural views showing the LSD1 catalytic site labeled by TCP and bound to either a wild-type SNAG peptide (left) or a modeled SNAG (F5A) peptide (right). Schematic of the protein domains of GFI1B highlighting the SNAG domain sequence (bottom). d, Binding curves showing fluorescence polarization (y axis) for increasing concentrations of LSD1–CoREST complex (x axis) in the presence of either wild-type GFI1B 2–10 peptide or GFI1B (F5A) 2–10 peptide (100 nM) and/or GSK-LSD1 (50 µM). Data represent mean ± s.e.m. across three technical replicates. One of two independent replicates is shown. e, Co-IP immunoblots showing levels of wild-type GFI1B–FLAG, GFI1B–FLAG (F5A) and LSD1 after anti-FLAG IP in SET-2 overexpressing wild-type GFI1B–FLAG or GFI1B–FLAG (F5A) after vehicle or GSK-LSD1 treatment (250 nM, 48 h). One of two independent replicates is shown. See Supplementary Fig. 7d for uncropped blot. f, Dose–response curves for SET-2 cells expressing wild-type GFI1B–FLAG or GFI1B–FLAG (F5A) treated with GSK-LSD1 are shown. Expression of GFI1B–FLAG (F5A) compared with wild-type GFI1B–FLAG significantly rescues growth of SET-2 cells. Data represent mean ± s.e.m. across three replicates. One of two independent replicates is shown.

Journal: Nature chemical biology

Article Title: CRISPR-suppressor scanning reveals a nonenzymatic role of LSD1 in AML.

doi: 10.1038/s41589-019-0263-0

Figure Lengend Snippet: Fig. 5 | An orthogonal drug-complementary GFI1B allele establishes sufficiency of the LSD1–GFI1B interaction for AML survival. a, Co-IP of wild-type FLAG–LSD1 and FLAG–LSD1 mutant variants with GFI1B was performed after vehicle or GSK-LSD1 treatment (250 nM, 48 h) in transiently transfected HEK 293T cells. Co-IP was performed using an anti-GFI1B antibody. LSD1 was detected using an anti-FLAG antibody. One of two independent replicates is shown. See Supplementary Fig. 7c for uncropped blot. b, Illustration depicting the concept of an orthogonal drug-complementary GFI1B allele that can only bind LSD1 in the presence of GSK-LSD1. c, Structural views showing the LSD1 catalytic site labeled by TCP and bound to either a wild-type SNAG peptide (left) or a modeled SNAG (F5A) peptide (right). Schematic of the protein domains of GFI1B highlighting the SNAG domain sequence (bottom). d, Binding curves showing fluorescence polarization (y axis) for increasing concentrations of LSD1–CoREST complex (x axis) in the presence of either wild-type GFI1B 2–10 peptide or GFI1B (F5A) 2–10 peptide (100 nM) and/or GSK-LSD1 (50 µM). Data represent mean ± s.e.m. across three technical replicates. One of two independent replicates is shown. e, Co-IP immunoblots showing levels of wild-type GFI1B–FLAG, GFI1B–FLAG (F5A) and LSD1 after anti-FLAG IP in SET-2 overexpressing wild-type GFI1B–FLAG or GFI1B–FLAG (F5A) after vehicle or GSK-LSD1 treatment (250 nM, 48 h). One of two independent replicates is shown. See Supplementary Fig. 7d for uncropped blot. f, Dose–response curves for SET-2 cells expressing wild-type GFI1B–FLAG or GFI1B–FLAG (F5A) treated with GSK-LSD1 are shown. Expression of GFI1B–FLAG (F5A) compared with wild-type GFI1B–FLAG significantly rescues growth of SET-2 cells. Data represent mean ± s.e.m. across three replicates. One of two independent replicates is shown.

Techniques: Co-Immunoprecipitation Assay, Mutagenesis, Transfection, Labeling, Sequencing, Binding Assay, Fluorescence, Western Blot, Expressing

Confirmation of mRNA expression of AR, JMJD2A, LSD1 in bladder cancer cell lines (A). Full length gels are presented in supplemental figure 1. The number of PCR cycles employed for each gene is indicated. GAPDH served as an internal control for cDNA integrity. Comparison of effects of 3mM and 1mM pargline and tranylcypromine (Tranyl) on proliferation of HTB-1 (B), HTB-5 (C), HTB-3 (D) and HT-1376 (E) bladder cancer cells. Quantitative RT-PCR was used to assess the effects of tranylcypromine on androgen regulated transcription (F). Neutral endopeptidase (NEP) is a representative AR-regulated gene expressed in both HTB1 and HTB5 bladder cancer cells. Bladder cells were treated with tranylcypromine (50µM) for 48 hours prior to transcriptional activation with the R1881 (1nM) synthetic androgen for 30 minutes. R1881 induces NEP expression in AR-positive HTB5 cells. This effect of R1881 on NEP expression in HTB5 cells is impaired by tranylcypromine. Neither R1881 nor tranylcypromine alter NEP expression in AR-negative HTB1 cells, suggesting the effects of tranylcypromine are dependent upon the presence of a functional AR-KDM complex.(*:p<0.05, ***p<0.01, ns: not significant).

Journal: Molecular Carcinogenesis

Article Title: Role of androgen receptor and associated lysine-demethylase coregulators, LSD1 and JMJD2A, in localized and advanced human bladder cancer

doi: 10.1002/mc.20758

Figure Lengend Snippet: Confirmation of mRNA expression of AR, JMJD2A, LSD1 in bladder cancer cell lines (A). Full length gels are presented in supplemental figure 1. The number of PCR cycles employed for each gene is indicated. GAPDH served as an internal control for cDNA integrity. Comparison of effects of 3mM and 1mM pargline and tranylcypromine (Tranyl) on proliferation of HTB-1 (B), HTB-5 (C), HTB-3 (D) and HT-1376 (E) bladder cancer cells. Quantitative RT-PCR was used to assess the effects of tranylcypromine on androgen regulated transcription (F). Neutral endopeptidase (NEP) is a representative AR-regulated gene expressed in both HTB1 and HTB5 bladder cancer cells. Bladder cells were treated with tranylcypromine (50µM) for 48 hours prior to transcriptional activation with the R1881 (1nM) synthetic androgen for 30 minutes. R1881 induces NEP expression in AR-positive HTB5 cells. This effect of R1881 on NEP expression in HTB5 cells is impaired by tranylcypromine. Neither R1881 nor tranylcypromine alter NEP expression in AR-negative HTB1 cells, suggesting the effects of tranylcypromine are dependent upon the presence of a functional AR-KDM complex.(*:p<0.05, ***p<0.01, ns: not significant).

Article Snippet: Primary antibodies for LSD1 (1B2E5, #NB-100-1762, Novus Biologicals), JMJD2A (# NB100-57563, Novus Biologicals) and AR (AM256, BioGenex) were detected using the Leica Microsystems Refine Detection Kit.

Techniques: Expressing, Control, Comparison, Quantitative RT-PCR, Activation Assay, Functional Assay

Association of JMJD2A, LSD1 and AR levels with patient clinicopathologic traits, disease recurrence and cancer-specific mortality in tumor specimens Fishers exact p-values are shown for each statistical association. Dark shading = significant (p <0.05). Superficial (Ta, T1, CIS) and muscle invasive (T2, T3, T4) bladder cancers. NMI:non muscle invasive; MI= muscle invasive ; BC: bladder confined, EVE; extravsical.

Journal: Molecular Carcinogenesis

Article Title: Role of androgen receptor and associated lysine-demethylase coregulators, LSD1 and JMJD2A, in localized and advanced human bladder cancer

doi: 10.1002/mc.20758

Figure Lengend Snippet: Association of JMJD2A, LSD1 and AR levels with patient clinicopathologic traits, disease recurrence and cancer-specific mortality in tumor specimens Fishers exact p-values are shown for each statistical association. Dark shading = significant (p <0.05). Superficial (Ta, T1, CIS) and muscle invasive (T2, T3, T4) bladder cancers. NMI:non muscle invasive; MI= muscle invasive ; BC: bladder confined, EVE; extravsical.

Techniques:

Representative immunohistochemical staining for AR (a-d), LSD1 (d-f) and JMJD2A (g-i)in benign urothelium, non-muscle invasive urothelial carcinoma (pTis, pTa, pT1), muscle invasive carcinoma (pT2) and extravesical (pT3) carcinoma. (All images taken at 400X total magnification; bar – 20 microns)

Journal: Molecular Carcinogenesis

Article Title: Role of androgen receptor and associated lysine-demethylase coregulators, LSD1 and JMJD2A, in localized and advanced human bladder cancer

doi: 10.1002/mc.20758

Figure Lengend Snippet: Representative immunohistochemical staining for AR (a-d), LSD1 (d-f) and JMJD2A (g-i)in benign urothelium, non-muscle invasive urothelial carcinoma (pTis, pTa, pT1), muscle invasive carcinoma (pT2) and extravesical (pT3) carcinoma. (All images taken at 400X total magnification; bar – 20 microns)

Techniques: Immunohistochemical staining, Staining

Kaplan-Meier overall survival estimates for 72 cystectomy patients, stratified by immunohistochemical staining positivity and intensity for AR (A-B), LSD1(C-D) and JMJD2A (E-F) in bladder tumors.

Journal: Molecular Carcinogenesis

Article Title: Role of androgen receptor and associated lysine-demethylase coregulators, LSD1 and JMJD2A, in localized and advanced human bladder cancer

doi: 10.1002/mc.20758

Figure Lengend Snippet: Kaplan-Meier overall survival estimates for 72 cystectomy patients, stratified by immunohistochemical staining positivity and intensity for AR (A-B), LSD1(C-D) and JMJD2A (E-F) in bladder tumors.

Techniques: Immunohistochemical staining, Staining

Correlation of levels of AR coregulators to levels of AR and to each other Expression of each marker was assessed for correlation using the Spearman rank correlation test. Spearman correlation coefficient and p values are shown for each correlation.

Journal: Molecular Carcinogenesis

Article Title: Role of androgen receptor and associated lysine-demethylase coregulators, LSD1 and JMJD2A, in localized and advanced human bladder cancer

doi: 10.1002/mc.20758

Figure Lengend Snippet: Correlation of levels of AR coregulators to levels of AR and to each other Expression of each marker was assessed for correlation using the Spearman rank correlation test. Spearman correlation coefficient and p values are shown for each correlation.

Techniques: Expressing, Marker

lsd1 function Search Results

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