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93
Bioss progesterone receptor
NGZT and SMX restore sex hormone balance and modulate the HPO axis. (A) Serum levels of <t>progesterone</t> in rats. (B) Serum levels of estradiol in rats. (C) Representative western blots of progesterone receptor (PR), estrogen receptor (ER), and oxytocin receptor (OTR) in the uterus. (D) Quantification of protein expression of PR, ER, and OTR in the uterus. (E) Quantification of mRNA expression of PR, ER, and OTR in the uterus. (F) Representative western blots of gonadotropin-releasing hormone receptor (GnRH-R) and GnRH in the ovaries. (G) Quantification of protein expression of GnRH-R and GnRH in the ovaries. (H) Quantification of mRNA expression of GnRH-R and GnRH in the ovaries. (I) Representative western blots of GnRH-R and GnRH in the hypothalami. (J) Quantification of protein expression of GnRH-R and GnRH in the hypothalami. (K) Quantification of mRNA expression of GnRH-R and GnRH in the hypothalami. Statistical significance was determined using one-way analysis of variance (ANOVA) followed by Tukey's multiple comparisons test.
Progesterone Receptor, supplied by Bioss, 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/progesterone+receptor+antibody/pmc13013513-99-28-32?v=Bioss
Average 93 stars, based on 1 article reviews
progesterone receptor - by Bioz Stars, 2026-08
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94
Novus Biologicals progesterone receptor
NGZT and SMX restore sex hormone balance and modulate the HPO axis. (A) Serum levels of <t>progesterone</t> in rats. (B) Serum levels of estradiol in rats. (C) Representative western blots of progesterone receptor (PR), estrogen receptor (ER), and oxytocin receptor (OTR) in the uterus. (D) Quantification of protein expression of PR, ER, and OTR in the uterus. (E) Quantification of mRNA expression of PR, ER, and OTR in the uterus. (F) Representative western blots of gonadotropin-releasing hormone receptor (GnRH-R) and GnRH in the ovaries. (G) Quantification of protein expression of GnRH-R and GnRH in the ovaries. (H) Quantification of mRNA expression of GnRH-R and GnRH in the ovaries. (I) Representative western blots of GnRH-R and GnRH in the hypothalami. (J) Quantification of protein expression of GnRH-R and GnRH in the hypothalami. (K) Quantification of mRNA expression of GnRH-R and GnRH in the hypothalami. Statistical significance was determined using one-way analysis of variance (ANOVA) followed by Tukey's multiple comparisons test.
Progesterone Receptor, 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/progesterone+receptor+antibody/pm41858165-82-51-58?v=Novus+Biologicals
Average 94 stars, based on 1 article reviews
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Cell Signaling Technology Inc dmso
A , Viability (ATP) of SKMES1, A549 cells, or A549 clones in which TXNDR1 is deleted, treated with BSO, with or without βMe (50 μM), or Fer-1 (10 μM), 3 days. Data report mean ± SEM of n=3 biological replicates. GI50 indicated. B , Growth of individual subcutaneous tumors derived from cell lines in A with or without BSO in drinking water (shaded region) reported as tumor volume (above) or change in tumor volume 21 days after start of BSO treatment or ethical endpoint if reached earlier (below). Data are individual tumor measurements. FD = animal found dead (data censored). P value reports result of Mann-Whitney U test. C , Summary of the impact of BSO on models tested. D , Schematic of chemical screen for suppressors of non-ferroptotic cell death mechanism. E , Z-score of viability (ATP) in SKMES1 cells treated with BSO (100 μM) with or without Fer-1 (10 <t>μM).</t> <t>Cycloheximide</t> (CHX) and erastin or erastin2 indicated (right only). Data report the mean of 2 technical replicates. F , Viability (ATP) of SKMES1 cells upon treatment with BSO, with <t>DMSO</t> or CHX (1 μM), 3 days. G , Viability (ATP) of SKMES1 cells upon treatment with BSO, with or without CySS supplementation (200 μM), βMe (50 μM), or Fer-1 (10 μM), 3 days. GI50 values from G reported in table at right. H , Viability (ATP) of SKMES1 cells upon CySS withdrawal and BSO treatment (100 μM), with or without βMe (50 μM), or Fer-1 (10 μM), 3 days. Data from F-H report mean ± SEM of n=3 biological replicates. I , Model describing the contribution of GSH and thioredoxin to ferroptosis the identified non-canonical cell death pathway, and its regulation by translation and cyst(e)ine availability.
Dmso, supplied by Cell Signaling Technology Inc, 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/progesterone+receptor+antibody/bio_rxiv__64898__2026__03__11__711115-175-42-44?v=Cell+Signaling+Technology+Inc
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96
Cell Signaling Technology Inc cell signaling technology 8757
A , Viability (ATP) of SKMES1, A549 cells, or A549 clones in which TXNDR1 is deleted, treated with BSO, with or without βMe (50 μM), or Fer-1 (10 μM), 3 days. Data report mean ± SEM of n=3 biological replicates. GI50 indicated. B , Growth of individual subcutaneous tumors derived from cell lines in A with or without BSO in drinking water (shaded region) reported as tumor volume (above) or change in tumor volume 21 days after start of BSO treatment or ethical endpoint if reached earlier (below). Data are individual tumor measurements. FD = animal found dead (data censored). P value reports result of Mann-Whitney U test. C , Summary of the impact of BSO on models tested. D , Schematic of chemical screen for suppressors of non-ferroptotic cell death mechanism. E , Z-score of viability (ATP) in SKMES1 cells treated with BSO (100 μM) with or without Fer-1 (10 <t>μM).</t> <t>Cycloheximide</t> (CHX) and erastin or erastin2 indicated (right only). Data report the mean of 2 technical replicates. F , Viability (ATP) of SKMES1 cells upon treatment with BSO, with <t>DMSO</t> or CHX (1 μM), 3 days. G , Viability (ATP) of SKMES1 cells upon treatment with BSO, with or without CySS supplementation (200 μM), βMe (50 μM), or Fer-1 (10 μM), 3 days. GI50 values from G reported in table at right. H , Viability (ATP) of SKMES1 cells upon CySS withdrawal and BSO treatment (100 μM), with or without βMe (50 μM), or Fer-1 (10 μM), 3 days. Data from F-H report mean ± SEM of n=3 biological replicates. I , Model describing the contribution of GSH and thioredoxin to ferroptosis the identified non-canonical cell death pathway, and its regulation by translation and cyst(e)ine availability.
Cell Signaling Technology 8757, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/progesterone+receptor+antibody/pm41803091-232-12-12?v=Cell+Signaling+Technology+Inc
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Cell Signaling Technology Inc anti pr
A , Viability (ATP) of SKMES1, A549 cells, or A549 clones in which TXNDR1 is deleted, treated with BSO, with or without βMe (50 μM), or Fer-1 (10 μM), 3 days. Data report mean ± SEM of n=3 biological replicates. GI50 indicated. B , Growth of individual subcutaneous tumors derived from cell lines in A with or without BSO in drinking water (shaded region) reported as tumor volume (above) or change in tumor volume 21 days after start of BSO treatment or ethical endpoint if reached earlier (below). Data are individual tumor measurements. FD = animal found dead (data censored). P value reports result of Mann-Whitney U test. C , Summary of the impact of BSO on models tested. D , Schematic of chemical screen for suppressors of non-ferroptotic cell death mechanism. E , Z-score of viability (ATP) in SKMES1 cells treated with BSO (100 μM) with or without Fer-1 (10 <t>μM).</t> <t>Cycloheximide</t> (CHX) and erastin or erastin2 indicated (right only). Data report the mean of 2 technical replicates. F , Viability (ATP) of SKMES1 cells upon treatment with BSO, with <t>DMSO</t> or CHX (1 μM), 3 days. G , Viability (ATP) of SKMES1 cells upon treatment with BSO, with or without CySS supplementation (200 μM), βMe (50 μM), or Fer-1 (10 μM), 3 days. GI50 values from G reported in table at right. H , Viability (ATP) of SKMES1 cells upon CySS withdrawal and BSO treatment (100 μM), with or without βMe (50 μM), or Fer-1 (10 μM), 3 days. Data from F-H report mean ± SEM of n=3 biological replicates. I , Model describing the contribution of GSH and thioredoxin to ferroptosis the identified non-canonical cell death pathway, and its regulation by translation and cyst(e)ine availability.
Anti Pr, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/progesterone+receptor+antibody/pm41790307-173-41-43?v=Cell+Signaling+Technology+Inc
Average 96 stars, based on 1 article reviews
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93
Santa Cruz Biotechnology progesterone receptor membrane component 1 pgrmc1
A , Viability (ATP) of SKMES1, A549 cells, or A549 clones in which TXNDR1 is deleted, treated with BSO, with or without βMe (50 μM), or Fer-1 (10 μM), 3 days. Data report mean ± SEM of n=3 biological replicates. GI50 indicated. B , Growth of individual subcutaneous tumors derived from cell lines in A with or without BSO in drinking water (shaded region) reported as tumor volume (above) or change in tumor volume 21 days after start of BSO treatment or ethical endpoint if reached earlier (below). Data are individual tumor measurements. FD = animal found dead (data censored). P value reports result of Mann-Whitney U test. C , Summary of the impact of BSO on models tested. D , Schematic of chemical screen for suppressors of non-ferroptotic cell death mechanism. E , Z-score of viability (ATP) in SKMES1 cells treated with BSO (100 μM) with or without Fer-1 (10 <t>μM).</t> <t>Cycloheximide</t> (CHX) and erastin or erastin2 indicated (right only). Data report the mean of 2 technical replicates. F , Viability (ATP) of SKMES1 cells upon treatment with BSO, with <t>DMSO</t> or CHX (1 μM), 3 days. G , Viability (ATP) of SKMES1 cells upon treatment with BSO, with or without CySS supplementation (200 μM), βMe (50 μM), or Fer-1 (10 μM), 3 days. GI50 values from G reported in table at right. H , Viability (ATP) of SKMES1 cells upon CySS withdrawal and BSO treatment (100 μM), with or without βMe (50 μM), or Fer-1 (10 μM), 3 days. Data from F-H report mean ± SEM of n=3 biological replicates. I , Model describing the contribution of GSH and thioredoxin to ferroptosis the identified non-canonical cell death pathway, and its regulation by translation and cyst(e)ine availability.
Progesterone Receptor Membrane Component 1 Pgrmc1, supplied by Santa Cruz Biotechnology, 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/progesterone+receptor+antibody/pm41671730-87-26-34?v=Santa+Cruz+Biotechnology
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86
Novocastra progesterone receptor
A , Viability (ATP) of SKMES1, A549 cells, or A549 clones in which TXNDR1 is deleted, treated with BSO, with or without βMe (50 μM), or Fer-1 (10 μM), 3 days. Data report mean ± SEM of n=3 biological replicates. GI50 indicated. B , Growth of individual subcutaneous tumors derived from cell lines in A with or without BSO in drinking water (shaded region) reported as tumor volume (above) or change in tumor volume 21 days after start of BSO treatment or ethical endpoint if reached earlier (below). Data are individual tumor measurements. FD = animal found dead (data censored). P value reports result of Mann-Whitney U test. C , Summary of the impact of BSO on models tested. D , Schematic of chemical screen for suppressors of non-ferroptotic cell death mechanism. E , Z-score of viability (ATP) in SKMES1 cells treated with BSO (100 μM) with or without Fer-1 (10 <t>μM).</t> <t>Cycloheximide</t> (CHX) and erastin or erastin2 indicated (right only). Data report the mean of 2 technical replicates. F , Viability (ATP) of SKMES1 cells upon treatment with BSO, with <t>DMSO</t> or CHX (1 μM), 3 days. G , Viability (ATP) of SKMES1 cells upon treatment with BSO, with or without CySS supplementation (200 μM), βMe (50 μM), or Fer-1 (10 μM), 3 days. GI50 values from G reported in table at right. H , Viability (ATP) of SKMES1 cells upon CySS withdrawal and BSO treatment (100 μM), with or without βMe (50 μM), or Fer-1 (10 μM), 3 days. Data from F-H report mean ± SEM of n=3 biological replicates. I , Model describing the contribution of GSH and thioredoxin to ferroptosis the identified non-canonical cell death pathway, and its regulation by translation and cyst(e)ine availability.
Progesterone Receptor, supplied by Novocastra, 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/progesterone+receptor+antibody/pmc12963160-25-14-19?v=Novocastra
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Cell Signaling Technology Inc pr b
A , Viability (ATP) of SKMES1, A549 cells, or A549 clones in which TXNDR1 is deleted, treated with BSO, with or without βMe (50 μM), or Fer-1 (10 μM), 3 days. Data report mean ± SEM of n=3 biological replicates. GI50 indicated. B , Growth of individual subcutaneous tumors derived from cell lines in A with or without BSO in drinking water (shaded region) reported as tumor volume (above) or change in tumor volume 21 days after start of BSO treatment or ethical endpoint if reached earlier (below). Data are individual tumor measurements. FD = animal found dead (data censored). P value reports result of Mann-Whitney U test. C , Summary of the impact of BSO on models tested. D , Schematic of chemical screen for suppressors of non-ferroptotic cell death mechanism. E , Z-score of viability (ATP) in SKMES1 cells treated with BSO (100 μM) with or without Fer-1 (10 <t>μM).</t> <t>Cycloheximide</t> (CHX) and erastin or erastin2 indicated (right only). Data report the mean of 2 technical replicates. F , Viability (ATP) of SKMES1 cells upon treatment with BSO, with <t>DMSO</t> or CHX (1 μM), 3 days. G , Viability (ATP) of SKMES1 cells upon treatment with BSO, with or without CySS supplementation (200 μM), βMe (50 μM), or Fer-1 (10 μM), 3 days. GI50 values from G reported in table at right. H , Viability (ATP) of SKMES1 cells upon CySS withdrawal and BSO treatment (100 μM), with or without βMe (50 μM), or Fer-1 (10 μM), 3 days. Data from F-H report mean ± SEM of n=3 biological replicates. I , Model describing the contribution of GSH and thioredoxin to ferroptosis the identified non-canonical cell death pathway, and its regulation by translation and cyst(e)ine availability.
Pr B, supplied by Cell Signaling Technology Inc, 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/progesterone+receptor+antibody/pmc12770934-90-48-49?v=Cell+Signaling+Technology+Inc
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Image Search Results


NGZT and SMX restore sex hormone balance and modulate the HPO axis. (A) Serum levels of progesterone in rats. (B) Serum levels of estradiol in rats. (C) Representative western blots of progesterone receptor (PR), estrogen receptor (ER), and oxytocin receptor (OTR) in the uterus. (D) Quantification of protein expression of PR, ER, and OTR in the uterus. (E) Quantification of mRNA expression of PR, ER, and OTR in the uterus. (F) Representative western blots of gonadotropin-releasing hormone receptor (GnRH-R) and GnRH in the ovaries. (G) Quantification of protein expression of GnRH-R and GnRH in the ovaries. (H) Quantification of mRNA expression of GnRH-R and GnRH in the ovaries. (I) Representative western blots of GnRH-R and GnRH in the hypothalami. (J) Quantification of protein expression of GnRH-R and GnRH in the hypothalami. (K) Quantification of mRNA expression of GnRH-R and GnRH in the hypothalami. Statistical significance was determined using one-way analysis of variance (ANOVA) followed by Tukey's multiple comparisons test.

Journal: Frontiers in Pain Research

Article Title: Integrated multi-omics elucidates the dual anti-inflammatory and neuroendocrine mechanisms of novel TCM plasters against primary dysmenorrhea

doi: 10.3389/fpain.2026.1727963

Figure Lengend Snippet: NGZT and SMX restore sex hormone balance and modulate the HPO axis. (A) Serum levels of progesterone in rats. (B) Serum levels of estradiol in rats. (C) Representative western blots of progesterone receptor (PR), estrogen receptor (ER), and oxytocin receptor (OTR) in the uterus. (D) Quantification of protein expression of PR, ER, and OTR in the uterus. (E) Quantification of mRNA expression of PR, ER, and OTR in the uterus. (F) Representative western blots of gonadotropin-releasing hormone receptor (GnRH-R) and GnRH in the ovaries. (G) Quantification of protein expression of GnRH-R and GnRH in the ovaries. (H) Quantification of mRNA expression of GnRH-R and GnRH in the ovaries. (I) Representative western blots of GnRH-R and GnRH in the hypothalami. (J) Quantification of protein expression of GnRH-R and GnRH in the hypothalami. (K) Quantification of mRNA expression of GnRH-R and GnRH in the hypothalami. Statistical significance was determined using one-way analysis of variance (ANOVA) followed by Tukey's multiple comparisons test.

Article Snippet: After blocking with 5% non-fat milk, the membranes were incubated overnight at 4 °C with primary antibodies against interleukin-6 (IL-6, 1:1000, Wanlei, WL02841), interleukin-1β (IL-1β, 1:1000, Affinity, AF5103), progesterone receptor (PR, 1:1000, Bioss, bs-23376R), cyclooxygenase-2 (COX-2, 1:2000, Proteintech, 66351-1-Ig), estrogen receptor (ER, 1:2000, Proteintech, 21244-1-AP), oxytocin receptor (OTR, 1:1500, Proteintech, 23045-1-AP), gonadotropin-releasing hormone receptor (GnRH-R, 1:1500, Proteintech, 22462-1-AP), and gonadotropin-releasing hormone (GnRH, 1:1000, Abclonal, A5625). β-actin (1:5000, TransGen, Q10410 ) or GAPDH (1:5000, TransGen, Q10614 ) served as the loading control.

Techniques: Western Blot, Expressing

A , Viability (ATP) of SKMES1, A549 cells, or A549 clones in which TXNDR1 is deleted, treated with BSO, with or without βMe (50 μM), or Fer-1 (10 μM), 3 days. Data report mean ± SEM of n=3 biological replicates. GI50 indicated. B , Growth of individual subcutaneous tumors derived from cell lines in A with or without BSO in drinking water (shaded region) reported as tumor volume (above) or change in tumor volume 21 days after start of BSO treatment or ethical endpoint if reached earlier (below). Data are individual tumor measurements. FD = animal found dead (data censored). P value reports result of Mann-Whitney U test. C , Summary of the impact of BSO on models tested. D , Schematic of chemical screen for suppressors of non-ferroptotic cell death mechanism. E , Z-score of viability (ATP) in SKMES1 cells treated with BSO (100 μM) with or without Fer-1 (10 μM). Cycloheximide (CHX) and erastin or erastin2 indicated (right only). Data report the mean of 2 technical replicates. F , Viability (ATP) of SKMES1 cells upon treatment with BSO, with DMSO or CHX (1 μM), 3 days. G , Viability (ATP) of SKMES1 cells upon treatment with BSO, with or without CySS supplementation (200 μM), βMe (50 μM), or Fer-1 (10 μM), 3 days. GI50 values from G reported in table at right. H , Viability (ATP) of SKMES1 cells upon CySS withdrawal and BSO treatment (100 μM), with or without βMe (50 μM), or Fer-1 (10 μM), 3 days. Data from F-H report mean ± SEM of n=3 biological replicates. I , Model describing the contribution of GSH and thioredoxin to ferroptosis the identified non-canonical cell death pathway, and its regulation by translation and cyst(e)ine availability.

Journal: bioRxiv

Article Title: Systematic Evaluation Defines the Limits of Ferroptosis in Cancer Therapy

doi: 10.64898/2026.03.11.711115

Figure Lengend Snippet: A , Viability (ATP) of SKMES1, A549 cells, or A549 clones in which TXNDR1 is deleted, treated with BSO, with or without βMe (50 μM), or Fer-1 (10 μM), 3 days. Data report mean ± SEM of n=3 biological replicates. GI50 indicated. B , Growth of individual subcutaneous tumors derived from cell lines in A with or without BSO in drinking water (shaded region) reported as tumor volume (above) or change in tumor volume 21 days after start of BSO treatment or ethical endpoint if reached earlier (below). Data are individual tumor measurements. FD = animal found dead (data censored). P value reports result of Mann-Whitney U test. C , Summary of the impact of BSO on models tested. D , Schematic of chemical screen for suppressors of non-ferroptotic cell death mechanism. E , Z-score of viability (ATP) in SKMES1 cells treated with BSO (100 μM) with or without Fer-1 (10 μM). Cycloheximide (CHX) and erastin or erastin2 indicated (right only). Data report the mean of 2 technical replicates. F , Viability (ATP) of SKMES1 cells upon treatment with BSO, with DMSO or CHX (1 μM), 3 days. G , Viability (ATP) of SKMES1 cells upon treatment with BSO, with or without CySS supplementation (200 μM), βMe (50 μM), or Fer-1 (10 μM), 3 days. GI50 values from G reported in table at right. H , Viability (ATP) of SKMES1 cells upon CySS withdrawal and BSO treatment (100 μM), with or without βMe (50 μM), or Fer-1 (10 μM), 3 days. Data from F-H report mean ± SEM of n=3 biological replicates. I , Model describing the contribution of GSH and thioredoxin to ferroptosis the identified non-canonical cell death pathway, and its regulation by translation and cyst(e)ine availability.

Article Snippet: L-buthionine sulfoximine (B2515), L-buthionine sulfoxide (SC-207795, Santa Cruz), L-methionine sulfoximine (AC227202500, Fisher Scientific), L-methionine sulfoxide (36255-1, Cayman Chemical), Cystine (C7602, Sigma), Erastin (S7242, Selleckchem), RSL-3 (HY-100218A, MedChemExpress), beta-mercaptoethanol (NC9604560, Fisher Scientific), ferrostatin-1 (SML0583, Sigma), cycloheximide (14126, Cayman), eprenetapopt (gift from Aprea Therapeutics), DMSO (3176, Cell Signaling Technologies), sodium selenite (214485, Sigma), doxycycline (J60579.22, LifeSciences), ML-162 (HY-100002, MedChemExpress) ML-210 (HY-100003, MedChemExpress), DTT (D0632, Sigma), TCEP (C4706, Sigma), U-13C-serine (CLM-1574-H, Cambridge Isotopes), Rosiglitazone (71740, Cayman), (R)-HTS-3 (37563, Cayman), GSH-Glo (Promega V6911), Cell Titer Glo (Promega G7573), Cell Death Inducer Compound Library (35093, Cayman), Transwell culture apparatus (CLS3464, Sigma).

Techniques: Clone Assay, Derivative Assay, MANN-WHITNEY