mProX™ Human GNRH1 Stable Cell Line
- Product Category:
- Membrane Protein Stable Cell Lines
- Subcategory:
- GPCR Cell Lines
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Published Data
Fig.1 A cellular line, engineered through CRISPR-Cas9 technology, has been established with GNRH1-TdTomato reporter capabilities.
The precise integration of an honor template into the genomic DNA of human pluripotent stem cells (hPSCs) was directed towards the final exon of GNRH1. This donor template was designed to encompass a T2A self-cleaving peptide and a nuclear localization signal (NLS), facilitating the cleavage and nuclear transport of the TdTomato protein, while preserving the integrity of the GnRH peptide.
Ref: Lund, Carina, et al. "Characterization of the human GnRH neuron developmental transcriptome using a GNRH1-TdTomato reporter line in human pluripotent stem cells." Disease models & mechanisms 13.3 (2020): dmm040105.
Pubmed: 37700498
DOI: 10.1080/15548627.2023.2254191
Research Highlights
Zhang H, et al. "Waterborne exposure to microcystin-leucine arginine induces endocrine disruption ." The Science of the total environment, 2023.
The impact of microcystins on gonad development and reproductive endocrine function in amphibian tadpoles (Pelophylax nigromaculatus) is not fully understood. To investigate this, tadpoles were exposed to 0, 1, and 10,ÄØmug/L of microcystin-leucine arginine (MC-LR) for 60,ÄØdays. Exposure to MC-LR resulted in changes to the structure of germ cells, specifically in oocytes. The 10,ÄØmug/L MC-LR group showed a significant decrease in female gonad size, but no significant difference in sex ratio. Gene transcription related to ovarian and testicular development was down-regulated after MC-LR exposure. Gonadotropin-releasing hormone transcripts were down-regulated in the hypothalamus, while gonadotropin levels increased in serum. Testosterone synthesis-related genes were up-regulated, leading to an increase in serum testosterone levels. However, a key gene involved in estrogen synthesis was down-regulated, resulting in lower estrogen levels. The down-regulation of vitellogenin gene transcription also suggests interference with the hypothalamic-pituitary-gonadal-liver axis. This study demonstrates the susceptibility of tadpole reproductive systems to the environmental risks of MC-LR.
Pubmed:
37806583
DOI:
10.1016/j.scitotenv.2023.167644
Tian Q, et al. "Idiopathic hypogonadotropic hypogonadism caused by compound heterozygosity for ." BMC endocrine disorders, 2023.
Idiopathic hypogonadotropic hypogonadism (IHH) is a rare genetic disorder caused by deficiency in gonadotropin-releasing hormone (GnRH). Patients with IHH are divided into two groups based on their sense of smell: hyposmic or anosmic (known as Kallmann syndrome) and normosmic IHH (nIHH). In this case report, a 15-year-old male with nIHH presented with delayed testicular development and low levels of testosterone and gonadotropins. Through genetic testing, novel compound heterozygous mutations in the GNRH1 gene, including a disruption of the start codon, were identified as the cause of the patient's nIHH. These findings expand the known mutations of GNRH1 and provide further insight into the genetic basis of nIHH.
Pubmed:
37798680
DOI:
10.1186/s12902-023-01455-7
