AMHR2 (Anti-Mullerian Hormone Receptor Type 2)

Among these, we identify the AMH-AMHR2 axis as a formerly unappreciated metastasis target. Thus, with StealTHY, we provide a new resource to expand the applicability of CRISPR screens to immunocompetent models, including humanized tumor grafts, revealing metastasis regulators of therapeutic relevance.

PepMLM-derived peptides demonstrate sequence-specific binding to cancer and reproductive targets, including NCAM1 and AMHR2, and enable targeted degradation of proteins across diverse disease contexts, from Huntington's disease to live viral infections. Altogether, PepMLM enables the design of candidate binders to any target protein, without requiring structural input, facilitating broad applications in therapeutic development.

The Silk-Ovarioids exhibited low intra-batch variability and long-term culture stability, underscoring their potential as a robust step toward developing a bioengineered, patient-specific artificial ovary. In addition, Silk-Ovarioids could be utilized as the first ovarian angiogenesis in vitro model, function as biological scaffold for in vitro folliculogenesis, and be used for toxicological and pharmacological studies targeting the ovaries.

Strong AMH, AMHR2, KISS1, and KISS1R expression suggests a potential role of these regulatory proteins in HLM pathophysiology. Further research on targeted modulation of these pathways may provide novel therapeutic approaches for BUMTs, particularly in cases where conventional treatments are limited.

A Amhr2-Cre; Foxl2+/C130W-FLEx mouse model recapitulates key aspects of the human AGCT including a dependence upon the causative FOXL2 mutation, concomitant uterine hyperplasia, and an age-dependent onset of tumors at the time of decreasing ovarian function. This new resource will accelerate translational research and therapeutic discovery for relapsed AGCT.

Retaining one testicle maintains endogenous testosterone production, thus avoiding imperfect hormonal replacement. Given the risk of tumoural degeneration, albeit a low one, annual imaging follow-up is mandatory and removal of Müllerian structures and gonadectomy may be considered if necessary.

In conclusion, MAbs for three different regions of AMHR2 were produced. One clone was shown to induce cytotoxicity in ovarian cancer cells and its sequence was determined for future use as a humanised therapeutic MAb.

Cells isolated from the mutant mice indicated that a subpopulation of cells marked by AMHR2-Cre:ROSA26 accounted for most cell growth and expansion in ovarian surface epithelial cells, and the AMHR2 lineage derived cells were regulated by AMH in vitro; whereas, fewer AMHR2-Cre:ROSA26 marked cells accounted for oviduct epithelial cell outgrowth. The results reveal a paracrine pathway in maintaining follicle-epithelial homeostasis in ovary and support a subpopulation of AMHR2 lineage marked epithelial cells as ovarian epithelial stem/progenitor cells with higher proliferative potential regulatable by follicle secreted AMH.

Consequently, it is involved in learning and memory processes and may support the treatment of Alzheimer's disease. This review aims to provide a comprehensive overview of the biology of AMH and its role in both endocrinology and oncology.

In lung adenocarcinoma tissues with high expression of AMHR2, activation of the AMH-AMHR2 pathway may suppress cell proliferation.

Three known synonymous variants with homozygous status were found in AMHR2. We conclude that the DNA variants identified in AMH and AMHR2 are not responsible for PMDS in the affected cat.

Using a dual fluorescence reporter line, the membrane-targeted tdTomato (mT)/membrane-targeted EGFP (mG) mouse, we provided evidence that Sertoli cells transdifferentiated toward a granulosa cell fate during tumorigenesis. Thus, our findings indicate that Sertoli cell-specific activation of TGFBR1 leads to the formation of TGCTs, supporting a key contribution of Sertoli cell reprogramming to the development of this testicular malignancy in our model.