PMID- 34321782
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20220304
IS  - 2455-1244 (Electronic)
IS  - 0971-913X (Print)
IS  - 0971-913X (Linking)
VI  - 21
IP  - 1
DP  - 2017 Jun
TI  - Membrane estrogen receptor 1 is required for normal reproduction in male and 
      female mice.
PG  - 1-14
AB  - Steroid hormones, acting through their cognate nuclear receptors, are critical 
      for many reproductive and non-reproductive functions. Over the past two decades, 
      it has become increasingly clear that in addition to cytoplasmic/nuclear steroid 
      receptors that alter gene transcription when liganded, a small fraction of 
      cellular steroid receptors are localized to the cell membranes, where they 
      mediate rapid steroid hormone effects. 17beta-Estradiol (E2), a key steroid hormone 
      for both male and female reproduction, acts predominately through its main 
      receptor, estrogen receptor 1 (ESR1). Most ESR1 is nuclear; however, 5-10% of 
      ESR1 is localized to the cell membrane after being palmitoylated at cysteine 451 
      in mice. This review discusses reproductive phenotypes of a newly-developed mouse 
      model with a C451A point mutation that precludes membrane targeting of ESR1. This 
      transgenic mouse, termed the nuclear-only ESR1 (NOER) mouse, shows extensive male 
      and female reproductive abnormalities and infertility despite normally functional 
      nuclear ESR1 (nESR1). These results provide the first in vivo evidence that 
      membrane-initiated E2/ESR1 signaling is required for normal male and female 
      reproductive functions and fertility. Signaling mechanisms for membrane ESR1 
      (mESR1), as well as how mESR1 works with nESR1 to mediate estrogen effects, are 
      still being established. We discuss some possible mechanisms by which mESR1 might 
      facilitate nESR1 signaling, as well as the emerging evidence that mESR1 might be 
      a major mediator of epigenetic effects of estrogens, which are potentially linked 
      to various adult-onset pathologies.
FAU - Nanjappa, Manjunatha K
AU  - Nanjappa MK
AD  - Department of Physiological Sciences, University of Florida, Gainesville, FL 
      32610, USA.
FAU - Mesa, Ana M
AU  - Mesa AM
AD  - Department of Physiological Sciences, University of Florida, Gainesville, FL 
      32610, USA.
FAU - Tevosian, Sergei G
AU  - Tevosian SG
AD  - Department of Physiological Sciences, University of Florida, Gainesville, FL 
      32610, USA.
FAU - de Armas, Laura
AU  - de Armas L
AD  - Department of Physiological Sciences, University of Florida, Gainesville, FL 
      32610, USA.
FAU - Hess, Rex A
AU  - Hess RA
AD  - Department of Comparative Biosciences, University of Illinois at 
      Urbana-Champaign, Urbana, IL, USA.
FAU - Bagchi, Indrani C
AU  - Bagchi IC
AD  - Department of Comparative Biosciences, University of Illinois at 
      Urbana-Champaign, Urbana, IL, USA.
FAU - Cooke, Paul S
AU  - Cooke PS
AD  - Department of Physiological Sciences, University of Florida, Gainesville, FL 
      32610, USA.
LA  - eng
GR  - R01 DK117633/DK/NIDDK NIH HHS/United States
GR  - R03 HD087528/HD/NICHD NIH HHS/United States
GR  - R21 HD088006/HD/NICHD NIH HHS/United States
PT  - Journal Article
PL  - India
TA  - J Endocrinol Reprod
JT  - Journal of endocrinology and reproduction : JER
JID - 9713097
PMC - PMC8315114
MID - NIHMS1652643
OTO - NOTNLM
OT  - 17beta-Estradiol
OT  - Efferent Ductules
OT  - Spermatogenesis
OT  - Testis
OT  - Uterus
EDAT- 2017/06/01 00:00
MHDA- 2017/06/01 00:01
PMCR- 2021/07/27
CRDT- 2021/07/29 06:45
PHST- 2021/07/29 06:45 [entrez]
PHST- 2017/06/01 00:00 [pubmed]
PHST- 2017/06/01 00:01 [medline]
PHST- 2021/07/27 00:00 [pmc-release]
PST - ppublish
SO  - J Endocrinol Reprod. 2017 Jun;21(1):1-14.