Affinage

PGR

Progesterone receptor · UniProt P06401

Round 2 corrected
Length
933 aa
Mass
99.0 kDa
Annotated
2026-04-28
130 papers in source corpus 36 papers cited in narrative 36 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

PGR encodes the progesterone receptor, a ligand-activated nuclear transcription factor that coordinates reproductive physiology—including ovulation, uterine decidualization, myometrial quiescence, and mammary gland development—by integrating genomic and non-genomic signaling. Two principal isoforms, PR-B and PR-A, are produced from distinct estrogen-regulated promoters: PR-B acts as the primary transcriptional activator by recruiting coactivators SRC-1, CBP, and pCAF to drive histone H4K5 acetylation at target promoters, whereas PR-A preferentially binds the corepressor SMRT and functions as a transdominant repressor of PR-B and other steroid receptors (PMID:2328727, PMID:10757795, PMID:12748280). Beyond classical genomic action, a polyproline motif in the PR N-terminus directly activates c-Src kinase via SH3-domain displacement to initiate rapid MAPK signaling (PMID:11545730); PR also physically associates with ERα to redirect its chromatin binding in breast cancer cells (PMID:26153859), suppresses NF-κB/COX-2 signaling through direct interaction with RelA and induction of IκBα (PMID:8626413, PMID:16772530), and a mitochondrial isoform (PR-M) localizes to the outer mitochondrial membrane where it increases cellular respiration (PMID:23518922). PR protein stability in the endometrium is controlled by P38α-mediated phosphorylation of the E3 ligase Ube3c, which restrains PR polyubiquitination and proteasomal degradation (PMID:35914132).

Mechanistic history

Synthesis pass · year-by-year structured walk · 23 steps
  1. 1987 High

    Determination of the complete primary sequence of human PR established it as a member of the nuclear receptor superfamily with a conserved cysteine-rich DNA-binding domain and a proline-rich N-terminal region, providing the molecular framework for all subsequent structure–function analysis.

    Evidence cDNA cloning and sequencing of the full 933-amino-acid open reading frame

    PMID:3551956

    Open questions at the time
    • No functional domains mapped beyond homology prediction
    • No information on isoform diversity
  2. 1989 High

    The discovery of two distinct nuclear localization mechanisms—a constitutive NLS and a ligand-dependent dimerization-mediated import—resolved how PR dynamically partitions between cytoplasm and nucleus before and after hormone exposure.

    Evidence Deletion mutagenesis of rabbit PR with dual-epitope immunofluorescence co-tracking

    PMID:2736623

    Open questions at the time
    • Chaperone involvement in cytoplasmic retention not addressed
    • Kinetics of nuclear import not quantified
  3. 1990 High

    Identification of two isoforms (PR-A and PR-B) produced from separate estrogen-regulated promoters, with distinct transactivation profiles on different promoters, established the principle of isoform-specific gene regulation that became central to PR biology.

    Evidence cDNA cloning, S1 nuclease mapping, primer extension, transient transfection reporter assays

    PMID:2328727

    Open questions at the time
    • Relative isoform ratios in different tissues not determined
    • Mechanisms governing isoform-specific activity unknown
  4. 1992 High

    Demonstrating direct PR–TFIIB interaction revealed that PR facilitates transcription in part by contacting the basal transcription machinery, providing a first mechanistic link between receptor binding and preinitiation complex assembly.

    Evidence Recombinant protein interaction assays and co-immunoprecipitation

    PMID:1517211

    Open questions at the time
    • Whether TFIIB contact is sufficient for activation or requires additional cofactors
    • Stoichiometry of interaction unknown
  5. 1995 High

    The discovery of SRC-1 as the first steroid receptor coactivator, identified through its direct interaction with PR, fundamentally changed understanding of nuclear receptor transcription by introducing the concept of ligand-dependent coactivator recruitment.

    Evidence Yeast two-hybrid screen with PR as bait, confirmed by co-transfection reporter assays and dominant-negative experiments

    PMID:7481822

    Open questions at the time
    • Which SRC family member is preferentially used by PR in vivo
    • Structural basis of SRC-1–PR interface unknown
  6. 1996 High

    Mutual trans-repression between PR and NF-κB/RelA, mediated by direct protein–protein interaction, established PR as an anti-inflammatory transcription factor independent of its classical hormone-response-element-driven gene activation.

    Evidence In vitro protein interaction assays with co-transfection reporter assays across multiple cell types

    PMID:8626413

    Open questions at the time
    • In vivo chromatin-level mechanism of mutual repression unresolved
    • Isoform-specificity of NF-κB repression not yet tested
  7. 1997 High

    Reconstitution of PR-dependent transcription in vitro, combined with evidence that pCAF and HDAC-1 antagonistically control PR transactivation, established histone acetylation/deacetylation as a core effector mechanism of PR-driven gene regulation.

    Evidence In vitro transcription assay, co-immunoprecipitation with pCAF, trichostatin A treatment and HDAC-1 co-expression

    PMID:9223281

    Open questions at the time
    • Specific histone residues targeted not identified
    • Whether pCAF and SRC-1 act in the same or parallel complexes unknown
  8. 1998 High

    The 1.8 Å crystal structure of the PR ligand-binding domain explained progesterone recognition through a conserved 3-oxy steroid mode, revealed a distinctive dimerization interface, and showed how anti-progestins like RU486 destabilize the activating C-terminal helix—providing the structural basis for agonist versus antagonist discrimination.

    Evidence X-ray crystallography at 1.8 Å resolution

    PMID:9620806

    Open questions at the time
    • Full-length receptor structure unavailable
    • N-terminal domain and DNA-binding domain structures unresolved
  9. 2000 High

    Differential cofactor selectivity—PR-A preferentially binding corepressor SMRT while PR-B efficiently recruits SRC-1/GRIP1—provided a molecular explanation for the opposing transcriptional activities of the two isoforms and showed that PR-A trans-repression and its inability to activate are mechanistically distinct.

    Evidence Phage display peptide selection, in vitro and in vivo cofactor interaction assays, dominant-negative SMRT mutants

    PMID:10757795

    Open questions at the time
    • Structural basis for differential SMRT versus coactivator binding unknown
    • Chromatin-level cofactor dynamics not addressed
  10. 2001 High

    Identification of a polyproline motif in the PR N-terminus that directly activates c-Src via SH3-domain displacement established that PR initiates rapid non-genomic signaling cascades (Src/MAPK) in addition to classical transcription, explaining progesterone effects too fast for gene regulation.

    Evidence SH3 domain pulldown, site-directed mutagenesis, kinase activity assays, Xenopus oocyte maturation assay

    PMID:11545730

    Open questions at the time
    • Downstream MAPK targets of non-genomic PR signaling not mapped
    • Relative contribution of genomic versus non-genomic pathways in specific tissues unknown
  11. 2001 High

    Genome-scale expression profiling in isogenic cell lines demonstrated that PR-A and PR-B regulate largely non-overlapping gene sets, transforming the view from quantitative differences in activation potency to qualitatively distinct transcriptional programmes.

    Evidence Microarray gene expression profiling in T47D cells expressing single PR isoforms

    PMID:11717311

    Open questions at the time
    • Chromatin occupancy differences between isoforms not yet mapped
    • Functional consequences of isoform-specific gene sets in vivo unclear
  12. 2003 High

    ChIP-based demonstration that ligand-activated PR preferentially recruits SRC-1 (over SRC-2) and CBP to drive H4K5 acetylation at target promoters provided the first histone-mark-level resolution of PR's chromatin remodeling mechanism.

    Evidence Chromatin immunoprecipitation, co-immunoprecipitation, dominant-negative experiments at MMTV-CAT reporter

    PMID:12748280

    Open questions at the time
    • Whether H4K5 acetylation is sufficient or simply correlative for PR-driven transcription
    • Additional histone marks at PR targets unexplored
  13. 2005 High

    Identification of AF3 (containing LXXLL motifs and Trp-140) in the PR-B-unique BUS segment showed that PR-B activates transcription through cooperative inter-domain synergy among multimers at tandem PREs—a mechanism fundamentally unavailable to PR-A—resolving why the two isoforms are not simply strong/weak versions of each other.

    Evidence Site-directed mutagenesis of LXXLL motifs and Trp-140, reporter assays, gene expression profiling

    PMID:16762974

    Open questions at the time
    • Structural model of inter-domain cooperation absent
    • Whether AF3 contacts specific coactivator surfaces directly is unresolved
  14. 2005 High

    Discovery that NF-κB drives expression of the truncated PR-C isoform in laboring myometrium, which in turn inhibits PR-B transactivation, established an inflammatory feed-forward loop that functionally withdraws progesterone action without changes in circulating hormone—a key concept for understanding human parturition.

    Evidence ChIP showing NF-κB binding to PR promoter, PR-C overexpression in myometrial cells, immunoblotting of laboring tissue

    PMID:16339279

    Open questions at the time
    • Mechanism by which PR-C inhibits PR-B at the molecular level not defined
    • Relevance to preterm labor not tested
  15. 2006 High

    Demonstration that PR suppresses NF-κB-driven COX-2 expression by blocking p65 promoter recruitment and rapidly inducing IκBα provided a direct molecular mechanism for progesterone's anti-inflammatory and uterine-quiescent effects, with ligand-independent PR activity shown by siRNA ablation.

    Evidence ChIP, siRNA knockdown, RT-PCR, Western blot, pharmacological antagonism with RU486 in myometrial cells

    PMID:16772530

    Open questions at the time
    • Whether ligand-independent repression operates through the same cofactor set as ligand-dependent repression
    • In vivo validation in conditional knockout models lacking
  16. 2006 High

    Bisulfite sequencing of endometriotic cells revealed that DNA methylation selectively silences the PR-B promoter while sparing PR-A, establishing an epigenetic mechanism for isoform-specific progesterone resistance in endometriosis.

    Evidence Laser capture microdissection, methylation-specific PCR, bisulfite sequencing of eutopic versus ectopic endometrium

    PMID:17965625

    Open questions at the time
    • Whether demethylating agents can restore PR-B and progesterone sensitivity in vivo
    • Upstream cause of selective PR-B promoter methylation unknown
  17. 2013 High

    Identification of PR-M as a mitochondrial outer membrane isoform that increases membrane potential and oxygen consumption in response to progestin revealed an entirely non-nuclear axis of progesterone signaling, expanding the receptor's functional repertoire beyond transcription.

    Evidence GFP fusion localization, immunoelectron microscopy, mitochondrial fractionation, mass spectrometry, oxygen consumption assays

    PMID:23518922

    Open questions at the time
    • Direct molecular target of PR-M on the outer mitochondrial membrane not identified
    • Physiological significance of PR-M in specific tissues not established
  18. 2015 High

    Genome-wide ChIP-seq showing that PR physically associates with ERα and redirects ERα chromatin binding to a unique gene programme associated with good clinical outcome reframed PR from a simple progesterone effector to a modulator of estrogen signaling in breast cancer.

    Evidence Reciprocal co-immunoprecipitation, ChIP-seq, xenograft growth assays, primary tumour explant cultures, genomic copy number analysis

    PMID:26153859

    Open questions at the time
    • Structural basis of PR–ERα interaction unknown
    • Whether PR-A or PR-B preferentially complexes with ERα not resolved
  19. 2015 High

    Demonstration that FOXO1 co-occupies >75% of PR binding sites in decidualizing endometrial stroma and is required for PR chromatin binding revealed a pioneering-factor-like dependency for PR in the endometrium.

    Evidence ChIP-seq, RNA-seq, siRNA knockdown of FOXO1 ablating PR binding

    PMID:25584414

    Open questions at the time
    • Whether FOXO1 directly opens chromatin for PR or acts via an intermediary unknown
    • Generalizability to other PR target tissues not tested
  20. 2015 High

    TALEN-mediated PGR knockout in zebrafish proved that nuclear PGR is essential for follicle rupture and ovulation but dispensable for oocyte meiotic maturation, genetically separating genomic PR function from the non-genomic progestin-triggered maturation pathway.

    Evidence TALEN gene knockout, in vivo/in vitro oocyte maturation assays, HCG and progestin treatment in zebrafish

    PMID:25852646

    Open questions at the time
    • Specific transcriptional targets of PGR required for follicle rupture not identified in this model
    • Mammalian generalizability assumed but not proven here
  21. 2016 High

    In vivo PGR knockdown in macaque granulosa cells prevented follicle rupture and the post-hCG progesterone rise, validating the zebrafish findings in a primate and revealing a positive feedback loop whereby nuclear PGR promotes its own ligand production during luteinization.

    Evidence Intra-follicular adenoviral shRNA injection, laparoscopic evaluation, serum hormone measurements

    PMID:26985003

    Open questions at the time
    • Downstream ovulatory genes controlled by PGR in primate not mapped genome-wide
    • Whether PR-A or PR-B mediates ovulation specifically is unknown
  22. 2022 High

    Discovery that P38α MAPK phosphorylates the E3 ligase Ube3c at Ser741 to restrain PR polyubiquitination and proteasomal degradation established the first complete post-translational pathway controlling PR protein turnover, with uterine P38α deletion causing PR loss, implantation failure, and infertility.

    Evidence Conditional knockout mice, co-immunoprecipitation, ubiquitination assays, Ube3c Ser741 mutagenesis, in vivo implantation phenotype

    PMID:35914132

    Open questions at the time
    • Whether this degradation pathway operates in breast or other PR-expressing tissues
    • Other E3 ligases targeting PR not excluded
  23. 2022 Medium

    In vivo PGR ChIP-seq in human myometrium showed that PGR genomic occupancy dynamically shifts from intergenic regions (not-in-labor) to promoter-proximal PREs (in-labor), with multi-omic integration identifying direct target genes including ATP11A and CBX7, providing the first genome-wide map of PR redistribution during parturition.

    Evidence ChIP-seq, RNA-seq, histone modification ChIP-seq in term human myometrium

    PMID:35732928

    Open questions at the time
    • Whether the cistrome shift is cause or consequence of labor onset
    • Functional validation of most newly identified target genes pending

Open questions

Synthesis pass · forward-looking unresolved questions
  • Despite extensive characterization of isoform-specific coactivator/corepressor recruitment, a full-length PR structure capturing the N-terminal domain, DNA-binding domain, and LBD in a single model is still lacking; the identity of PR-M's direct mitochondrial binding partner and the structural basis of the PR–ERα complex remain undefined; and whether the dynamic cistrome redistribution observed in laboring myometrium is a cause or consequence of parturition requires time-resolved manipulation.
  • No full-length PR structural model exists
  • PR-M's direct mitochondrial target unknown
  • Structural basis of PR–ERα interaction unresolved
  • Causal role of PR cistrome shift in labor initiation not established

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140110 transcription regulator activity 7 GO:0098772 molecular function regulator activity 6 GO:0003677 DNA binding 5
Localization
GO:0005634 nucleus 5 GO:0005654 nucleoplasm 3 GO:0005739 mitochondrion 1
Pathway
R-HSA-74160 Gene expression (Transcription) 7 R-HSA-162582 Signal Transduction 5 R-HSA-1474165 Reproduction 4 R-HSA-168256 Immune System 3
Partners
ARID1ACREBBPESR1FOXO1KAT2BRELASMRTSRC1

Evidence

Reading pass · 36 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1990 The human progesterone receptor (hPR) gene encodes two protein isoforms, PR-A and PR-B, generated from two distinct estrogen-regulated promoters; PR-A initiates from an internal promoter producing a transcript lacking the 5' region upstream of AUG1, while PR-B initiates from an upstream promoter. Both isoforms similarly activate transcription from a single palindromic PRE, but PR-B is more efficient at activating the MMTV LTR PRE, while PR-A (but not PR-B) induces transcription from the ovalbumin promoter. cDNA cloning, S1 nuclease mapping, primer extension, transient transfection reporter assays The EMBO journal High 2328727
1987 The complete amino acid sequence of the human progesterone receptor was determined from cloned cDNA; the protein is 933 amino acids with a cysteine-rich DNA-binding domain homologous to other nuclear receptors and a high proline content in the N-terminal region. cDNA library screening, sequencing of overlapping clones Biochemical and biophysical research communications High 3551956
1998 The 1.8 Å crystal structure of the progesterone-bound ligand-binding domain (LBD) of human PR revealed that progesterone is recognized via a 3-oxy steroid mode shared with related receptors, that PR uses a distinctive dimerization interface compared to related receptors, and that ligand-induced stabilization of the C-terminal helix of the LBD accounts for protease resistance and loss of repression; the structure also indicated how the anti-progestin RU486 disrupts this stabilization. X-ray crystallography at 1.8 Å resolution Nature High 9620806
1995 Steroid receptor coactivator-1 (SRC-1) was identified as a direct binding partner of human PR that enhances PR transcriptional activity without altering basal promoter activity; SRC-1 coactivates all steroid receptors tested; an amino-terminal truncation of SRC-1 acts as a dominant-negative repressor, and SRC-1 reversed ER-mediated squelching of PR activation. Yeast two-hybrid interaction screen, co-transfection reporter assays, dominant-negative repressor experiments Science High 7481822
1992 PR directly interacts with the general transcription factor TFIIB (S300-II) via protein-protein interaction, indicating that PR facilitates transcription at least in part by contacting the basal transcription machinery. Protein-protein interaction assays with recombinant proteins, co-immunoprecipitation The Journal of biological chemistry High 1517211
1996 The RelA (p65) subunit of NF-κB and PR mutually repress each other's transcriptional activity; this trans-repression is independent of PR isoform, reporter construct, or cell type and is mediated by direct protein-protein interaction between PR and RelA demonstrated in vitro. Co-transfection reporter assays, in vitro protein interaction assays The Journal of biological chemistry High 8626413
1998 HMG-1 and HMG-2 stimulate the sequence-specific DNA binding activity of PR in vitro by forming a ternary HMG-PR-DNA complex through transient protein-protein interaction combined with DNA structure recognition; HMG-1/-2 coexpression increased PR-mediated transcription up to 7–10-fold in mammalian cells without altering basal promoter activity. In vitro DNA binding assays, gel shift/ternary complex analysis, transient transfection reporter assays Molecular and cellular biology High 9671457
1999 E6-AP (UBE3A) directly interacts with PR in a hormone-dependent manner and coactivates PR transcriptional activity; the ubiquitin-protein ligase function of E6-AP is dispensable for coactivation, demonstrating two separable independent functions of E6-AP. Direct protein interaction assays, co-transfection reporter assays, mutant E6-AP analysis Molecular and cellular biology High 9891052
2000 The two PR isoforms (hPRA and hPRB) exhibit differential cofactor binding: hPRA has higher affinity for the corepressor SMRT (mediated by an inhibitory domain, ID) and fails to efficiently recruit coactivators GRIP1 and SRC-1 upon agonist binding, whereas hPRB efficiently recruits coactivators; inhibition of SMRT reverses hPRA-mediated transrepression but does not convert hPRA to a transcriptional activator, indicating that the inability to activate and the ability to transrepress occur by distinct mechanisms. Phage display peptide selection, in vitro and in vivo cofactor interaction assays, dominant-negative SMRT mutants, HDAC inhibitor experiments Molecular and cellular biology High 10757795
2001 PR contains a specific polyproline motif in its amino-terminal domain that mediates direct, progestin-dependent interaction with SH3 domains of cytoplasmic signaling molecules including c-Src tyrosine kinases via an SH3-domain displacement mechanism; mutagenesis of this motif abolished rapid progestin-induced Src and MAP kinase activation and affected progestin-induced growth arrest and Xenopus oocyte maturation, indicating a non-genomic PR signaling pathway. SH3 domain pulldown, site-directed mutagenesis, kinase activity assays, Xenopus oocyte maturation assay Molecular cell High 11545730
2001 PR-A and PR-B regulate largely distinct gene sets in human breast cancer cells: of 94 progesterone-regulated genes identified, 65 are uniquely regulated by PR-B, 4 uniquely by PR-A, and only 25 by both isoforms. Microarray gene expression profiling in isogenic cell lines expressing one PR isoform The Journal of biological chemistry High 11717311
2003 PR preferentially recruits SRC-1 (rather than SRC-2) upon ligand activation, which subsequently recruits CBP and leads to enhanced acetylation specifically at K5 of histone H4; this differential coactivator recruitment determines the specificity of chromatin modification at progesterone-responsive promoters. Chromatin immunoprecipitation, co-immunoprecipitation, loss-of-function (dominant-negative) experiments with MMTV-CAT reporter Molecular and cellular biology High 12748280
1997 PR-driven transcription requires SRC-1A coactivator (shown by dominant-negative inhibition in an in vitro transcription assay); PR also interacts with p300/CBP-associated factor (pCAF) in vitro; histone deacetylase inhibition potentiates PR-driven transcription while recruiting HDAC-1 to the PR-DNA complex represses it, indicating that targeted histone acetylation/deacetylation is a key mechanism controlling PR transactivation. In vitro transcription assay, co-immunoprecipitation, transient transfection reporter assays with HDAC-1 and trichostatin A Proceedings of the National Academy of Sciences of the United States of America High 9223281
2003 IGF-I inhibits PR mRNA and protein expression in breast cancer cells via the PI3K/Akt/mTOR pathway by suppressing PR gene transcription (not via proteasome-mediated degradation); this effect is independent of estrogen receptor levels or activity, as constitutively active PI3K or Akt induced ER activity while reducing PR levels. RT-PCR, Western blot, pharmacological inhibitors of PI3K/Akt/mTOR, constitutively active kinase constructs, proteasome inhibitor controls Molecular endocrinology High 12554765
2005 PR-B and PR-A regulate transcription by fundamentally different mechanisms: the B-upstream segment (BUS) of PR-B contains a unique activation function AF3 with two LXXLL motifs plus Trp-140 that synergizes with downstream AF1 and AF2 through cooperative interactions among receptor multimers bound at tandem hormone response elements; mutation of AF3 (PR-BdL140) completely destroys PR-B activity without converting it to a PR-A-like receptor. Site-directed mutagenesis of LXXLL motifs and Trp140, reporter gene transactivation assays, gene expression profiling of stable cell lines Molecular endocrinology High 16762974
2005 Up-regulation of the truncated PR-C isoform in laboring myometrium by NF-κB pathway activation inhibits PR-B transactivation; chromatin immunoprecipitation showed IL-1β-induced binding of NF-κB to the PR promoter, and overexpression of PR-C in myometrial cells inhibited PR-B transcriptional activity. Immunoblotting, quantitative PCR, overexpression in myometrial cells, chromatin immunoprecipitation Molecular endocrinology High 16339279
2006 PR inhibits NF-κB activation of COX-2 gene expression in myometrial cells via both ligand-dependent and ligand-independent mechanisms; progesterone treatment suppressed IL-1β-induced NF-κB p65 recruitment to COX-2 promoter elements (shown by ChIP) and rapidly induced IκBα mRNA and protein; siRNA ablation of both PR isoforms enhanced NF-κB activation and COX-2 expression even without exogenous progesterone. Chromatin immunoprecipitation, siRNA knockdown, RT-PCR, Western blot, pharmacological antagonism (RU486) Molecular endocrinology High 16772530
2006 Promoter hypermethylation of the PR-B (but not PR-A) promoter in endometriotic epithelial cells silences PR-B expression, establishing epigenetic regulation as a mechanism for isoform-specific progesterone resistance in endometriosis. Laser capture microdissection, methylation-specific PCR, bisulfite sequencing Epigenetics High 17965625
2006 Two novel membrane progesterone receptors (mPRα and mPRβ) are present in human myometrium, are coupled to inhibitory G proteins causing cAMP decline and increased myosin light chain phosphorylation to facilitate contraction, and activation of mPRs leads to transactivation of nuclear PR-B — the first evidence for cross-talk between membrane and nuclear PRs; mPRs also decrease steroid receptor coactivator 2. Receptor binding assays, G-protein coupling (cAMP measurement), myosin light chain kinase assays, co-immunoprecipitation, reporter transactivation assays Molecular endocrinology High 16484338
2007 Chromosome-targeted duplex RNAs complementary to the PR promoter activate PR expression in breast cancer cells; chromatin immunoprecipitation showed that activation is accompanied by reduced acetylation at histones H3K9 and H3K14 and increased di- and trimethylation at H3K4 at the PR promoter. Transfection of promoter-targeted duplex RNAs, chromatin immunoprecipitation for histone marks Nature chemical biology Medium 17259978
2013 A truncated progesterone receptor isoform, PR-M, encoded by a sequence in the distal third intron of the PGR gene fused to exons 4–8, localizes to the outer mitochondrial membrane (confirmed by immunofluorescence of PR-M-GFP fusion, immunoelectron microscopy, mitochondrial fractionation, and mass spectrometry); removal of the N-terminal mitochondrial localization signal abolished mitochondrial association; overexpression of PR-M increased mitochondrial membrane potential and oxygen consumption in response to progestin, indicating direct regulation of cellular respiration. GFP fusion protein localization, immunoelectron microscopy, mitochondrial fractionation Western blot, mass spectrometry, oxygen consumption assay, gene silencing Molecular endocrinology High 23518922
2015 PR associates with ERα protein in the presence of agonist ligands to direct ERα chromatin binding events within breast cancer cells, producing a unique gene expression programme associated with good clinical outcome; progesterone inhibited oestrogen-mediated growth of ERα+ xenografts and primary tumour explants; copy number loss of PGR is common in ERα+ breast cancers, explaining reduced PR in a subset of cases. Co-immunoprecipitation, ChIP-seq, xenograft experiments, primary tumour explant cultures, genomic copy number analysis Nature High 26153859
2015 FOXO1 is functionally required for PR binding to genomic targets during decidualization; ablation of FOXO1 abolishes PR binding to a shared binding interval downstream of the IRF4 gene; FOXO1 and PR co-occupy more than 75% of PR ChIP-seq intervals in human endometrial stromal cells, and IRF4 is a downstream target of both FOXO1 and PR required for decidualization. ChIP-seq, RNA-seq, siRNA knockdown, reporter assays Molecular endocrinology High 25584414
2015 Nuclear PGR knockout in zebrafish using TALENs showed that Pgr is essential for follicle rupture and ovulation but is not required for meiosis resumption or germinal vesicle breakdown; homozygous Pgr-KO female fish are infertile due to anovulation despite normal oocyte maturation in vitro. TALEN-mediated gene knockout, in vivo and in vitro oocyte maturation assays, HCG and progestin treatment Frontiers in endocrinology High 25852646
2016 Adenoviral shRNA-mediated knockdown of PGR in macaque granulosa cells prevented follicle rupture in 5 of 6 monkeys following hCG administration, with a trapped oocyte confirmed; PGR knockdown also prevented the rise in serum progesterone following hCG, suggesting that nuclear PGR promotes its own synthesis by facilitating luteinization and progesterone production. Adenoviral shRNA knockdown in vivo (intra-follicular injection), laparoscopic evaluation, hormone measurement, immunohistochemistry Biology of reproduction High 26985003
2017 Ligand-activated PR represses interferon-stimulated gene (ISG) transcription in breast cancer cells by being recruited to ISG enhancer regions (demonstrated by ChIP) and impairing recruitment of STAT2 and IRF9 to ISG promoters; ligand-independent regulation was also observed, as PR knockdown markedly increased basal ISG transcript levels. ChIP-seq/ChIP, siRNA knockdown, IFN treatment, RT-PCR and RNA-seq Molecular cancer research Medium 28684637
2019 Dynamic PGR cistrome profiling in human myometrium revealed that PGR genome occupancy shifts significantly between non-pregnant and term-pregnant states, with PGR predominantly occupying promoter regions (including classical PREs) in labor tissue versus intergenic regions in non-labor tissue; PGR co-occupying sites are enriched for SRF, MYOD, and STAT binding motifs, suggesting interactions between PGR and muscle regulators. ChIP-seq (PGR), ATACseq (accessible chromatin), RNA-seq, motif enrichment analysis FASEB journal Medium 31908010
2018 FOS expression in human periovulatory follicles is induced by collaborative actions of PGR and EGF receptor signaling after hCG; PGR binds directly to the FOS gene (shown by ChIP); FOS then binds to promoter regions of prostaglandin synthases and transporters (PTGES, SLCO2A1, ABCC1); pharmacological inhibition of PGR or EGFR reduced hCG-induced FOS expression and phosphorylation. Chromatin immunoprecipitation, pharmacological inhibition of PGR and EGFR, RT-PCR, Western blot, prostaglandin measurement The Journal of clinical endocrinology and metabolism Medium 30124866
2019 miR-375 targets PGR mRNA in bovine cumulus cells, verified by dual-luciferase reporter assay and RNA immunoprecipitation; PGR knockdown repressed cumulus-oocyte complex maturation, and restoration of PGR expression abated miR-375 overexpression-mediated suppression of maturation. Dual-luciferase reporter assay, RNA immunoprecipitation, lentiviral miR-375 overexpression/knockdown, Western blot Biomedicine & pharmacotherapy Medium 31545267
2021 ARID1A physically interacts with PR-A (but not PR-B) in mouse and human endometrium, demonstrated by co-immunoprecipitation and proximity ligation assay; ARID1A and PGR co-localize in the epithelium during proliferative and early secretory phases. Co-immunoprecipitation, proximity ligation assay, immunohistochemistry, Western blot Biochemical and biophysical research communications Medium 33706098
2022 P38α MAPK maintains PR protein stability in the endometrium by phosphorylating the E3 ubiquitin ligase Ube3c at serine 741, which restrains Ube3c-mediated polyubiquitination and proteasomal degradation of PR; uterine-selective P38α depletion caused dramatic PR protein down-regulation in stromal cells, defective implantation, and female infertility. Conditional knockout mice, co-immunoprecipitation, ubiquitination assays, site-directed mutagenesis of Ube3c Ser741, in vivo implantation phenotype Proceedings of the National Academy of Sciences of the United States of America High 35914132
2022 In vivo genome-wide PGR ChIP-seq in human myometrial tissue from term pregnant in-labor vs. not-in-labor subjects showed that PGR binding shifts from intergenic sites (not in labor) to promoter regions including classical PREs (in labor); three-way data integration identified ATP11A, CBX7, and TNS1 as direct PGR target genes with altered expression and active histone marks during labor. ChIP-seq (PGR), RNA-seq, histone modification ChIP-seq, in vitro progesterone response validation Reproductive sciences Medium 35732928
2025 H3K27ac loss is mechanistically linked to reduced PGR expression in aging endometrium; elimination of H3K27ac in young human endometrial stromal cells caused reduced PGR levels, and the H3K27ac/PGR relationship was validated in a mouse aging model, establishing H3K27ac as a critical upstream epigenetic regulator of PGR. Transcriptomic profiling, H3K27ac inhibition in primary stromal cells, Western blot, mouse model validation Nature aging Medium 40394215
1989 Nuclear localization of the progesterone receptor is mediated by two distinct mechanisms: a constitutively active nuclear localization signal around amino acids 638-642 (homologous to SV40 large T antigen NLS), and a ligand-dependent mechanism involving activation of the DNA-binding domain; in the absence of ligand, receptor is transferred to the nucleus as a monomer, but after hormone administration a cytoplasmic monomer is transferred through interaction with a nuclear monomer via the steroid-binding domains. Deletion mutagenesis of rabbit PR, immunofluorescence co-tracking of receptor mutants with distinct epitope tags in the same cells Cell High 2736623
2012 PGR plays a critical role in ovulation in mammals: PGR is highly expressed in granulosa cells of preovulatory follicles in response to the LH surge and mediates downstream gene regulation required for oocyte release, while also being expressed in oviductal epithelial and muscle cells to regulate oviductal transport. Review integrating PGR knockout mouse data, immunolocalization, and gene expression studies (summary of prior functional evidence) Reproduction in domestic animals Medium 22827383
2012 ATBF1 transcription factor is a direct transcriptional target of the progesterone-PR signaling pathway in mammary epithelial cells; promoter-reporter and ChIP assays showed that progesterone-activated PR directly binds the ATBF1 promoter; ATBF1 induction is required for PR-driven progenitor cell transition (colony formation in Matrigel and stem cell marker expression). RT-PCR, Western blot, promoter-reporter assay, ChIP, siRNA knockdown, Matrigel colony formation assay Biochemical and biophysical research communications Medium 23159610

Source papers

Stage 0 corpus · 130 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1995 Sequence and characterization of a coactivator for the steroid hormone receptor superfamily. Science (New York, N.Y.) 1979 7481822
2009 Ki67 index, HER2 status, and prognosis of patients with luminal B breast cancer. Journal of the National Cancer Institute 1642 19436038
1990 Two distinct estrogen-regulated promoters generate transcripts encoding the two functionally different human progesterone receptor forms A and B. The EMBO journal 1331 2328727
2009 A census of human transcription factors: function, expression and evolution. Nature reviews. Genetics 1191 19274049
2021 Dual proteome-scale networks reveal cell-specific remodeling of the human interactome. Cell 705 33961781
2011 Phylogenetic-based propagation of functional annotations within the Gene Ontology consortium. Briefings in bioinformatics 656 21873635
2009 Breast cancer subtypes based on ER/PR and Her2 expression: comparison of clinicopathologic features and survival. Clinical medicine & research 633 19574486
1998 Atomic structure of progesterone complexed with its receptor. Nature 539 9620806
2015 Progesterone receptor modulates ERα action in breast cancer. Nature 532 26153859
2008 Plant pathogenesis-related (PR) proteins: a focus on PR peptides. Plant physiology and biochemistry : PPB 489 18674922
2000 Structural evidence for ligand specificity in the binding domain of the human androgen receptor. Implications for pathogenic gene mutations. The Journal of biological chemistry 481 10840043
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