Paige Steffen

ORCID: 0000-0003-2505-0082
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About
Contact & Profiles
Research Areas
  • Plant Reproductive Biology
  • Hypothalamic control of reproductive hormones
  • Ovarian function and disorders
  • Genomics and Chromatin Dynamics
  • Developmental Biology and Gene Regulation
  • Plant Molecular Biology Research
  • Hedgehog Signaling Pathway Studies
  • Neuropeptides and Animal Physiology
  • Genomic variations and chromosomal abnormalities
  • Education Discipline and Inequality
  • Child and Adolescent Psychosocial and Emotional Development
  • Bullying, Victimization, and Aggression
  • Congenital limb and hand anomalies

University of California, San Diego
2021-2024

Loyola University Chicago
2015

Enhancers control the location and timing of gene expression contain majority variants associated with disease

10.1038/s41586-023-06922-8 article EN cc-by Nature 2024-01-17

Kisspeptin, encoded by Kiss1, stimulates gonadotropin-releasing hormone neurons to govern reproduction. In female rodents, estrogen-sensitive kisspeptin in the rostral anteroventral periventricular (AVPV) hypothalamus are thought mediate estradiol (E2)-induced positive feedback induction of preovulatory luteinizing (LH) surge. AVPV coexpress estrogen and progesterone receptors (PGRs) activated during LH While E2 effects on have been well studied, progesterone's regulation is less understood....

10.1210/endocr/bqab161 article EN Endocrinology 2021-08-11

Abstract Classic pharmacological studies suggested that endogenous dynorphin-KOR signaling is important for reproductive neuroendocrine regulation. With the seminal discovery of an interconnected network hypothalamic arcuate neurons co-expressing kisspeptin, neurokinin B, and dynorphin (KNDy neurons), KNDy hypothesis was developed to explain how gonadotropin-releasing hormone (GnRH) luteinizing (LH) pulses are generated. Key this released from acting in a paracrine manner on other via kappa...

10.1210/endocr/bqac175 article EN Endocrinology 2022-10-19

Abstract Puberty is the critical developmental transition to reproductive capability driven by activation of gonadotropin‐releasing hormone (GnRH) neurons. The complex neural mechanisms underlying pubertal GnRH secretion still remain unknown, yet likely include kisspeptin However, neurons reside in several hypothalamic areas and specific population timing onset remains undetermined. To investigate this, we strategically capitalized on differential ontological expression Kiss1 gene different...

10.1096/fj.202401696r article EN cc-by-nc The FASEB Journal 2024-10-08

Summary An emerging regulatory principle governing enhancers is the use of suboptimal affinity binding sites to encode tissue-specific gene expression. Here we investigate if optimizing single-nucleotide variants that violate this can disrupt expression and development. The ZRS enhancer mediates Shh in posterior developing limb buds critical for digit We find contains suboptimal-affinity ETS sites. Two human mutations a synthetic mutation optimize ETS-A site from 0.15 0.25 relative cause...

10.1101/2022.05.27.493789 preprint EN cc-by-nc bioRxiv (Cold Spring Harbor Laboratory) 2022-05-28

Abstract Puberty is a crucial period of transition to adulthood, marked by an increased activation gonadotropin-releasing hormone (GnRH) neurons that drives pulsatile secretion pituitary luteinizing (LH). The mechanisms governing GnRH neuron at puberty remain unclear but are likely due enhanced signaling from upstream populations, including kisspeptin neurons. Kisspeptin (encoded Kiss1) directly stimulates drive release and downstream LH secretion. Humans animals with Kiss1 mutations fail...

10.1210/jendso/bvab048.1093 article EN cc-by-nc-nd Journal of the Endocrine Society 2021-05-01
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