AMH Gene anti-Mullerian hormone

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Known as:: AMH Gene (anti-) to-Mullerian hormone
Catalog number:: AMICA1
Category:: -
Supplier:: Transposagen
Gene target:: AMH Gene anti-Mullerian hormone

Related genes to: AMH Gene anti-Mullerian hormone

Gene:: FOXD3 ^{NIH gene}
Name:: forkhead box D3
Previous symbol:: -
Synonyms:: Genesis, HFH2
Chromosome:: 1p31.3
Locus Type:: gene with protein product
Date approved:: 1999-12-22
Date modifiied:: 2015-08-25

Related products to: AMH Gene anti-Mullerian hormone

Related articles to: AMH Gene anti-Mullerian hormone

OTUB2/ALYREF axis modulates the docetaxel resistance of castration-resistant prostate cancer via upregulating ABCG4-mediated drug efflux.
Docetaxel (DTX) is a standard chemotherapy agent for castration-resistant prostate cancer (CRPC); however, DTX resistance remains a major clinical challenge, and the underlying molecular mechanisms are not fully understood. In our study, it was found that OTUB2 was highly expressed in DTX-resistant CRPC and could be served as a key driver of DTX resistance. Mechanistically, OTUB2 stabilizes the m5C reader ALYREF by removing its K48-linked polyubiquitin chains, leading to increased ALYREF protein levels. And then, ALYREF enhances the mRNA stability and expression of ABCG4, thereby promoting ATP-dependent efflux of DTX. Moreover, the expression of OTUB2 mRNA and protein could be regulated by FOXD3-AS1 derived from cancer-associated fibroblasts (CAFs). More importantly, treatment with OTUB2 inhibitor (OTUB2-IN-1) resensitized resistant CRPC to DTX. Together, our findings establish OTUB2 as a novel driver of DTX resistance in CRPC and highlight the role of CAFs-derived FOXD3-AS1 and OTUB2/ALYREF/ABCG4 axis in modulating DTX resistance of CRPC. - Source: PubMed
Publication date: 2026/03/17
Ke Zhi-BinChen Jia-YinLin BinChen Chao-RanXue Yu-TingSun Jiang-BoYan Zi-HengZhao Yu-XuanLiu Meng-XinWang ZhenXue Xue-YiZheng Qing-ShuiWei YongXu Ning
Dynamic and non-uniform expression of key transcription factors provides insights into the emergence of neural crest cells at the neural plate border.
The neural crest is a vertebrate stem cell population with broad developmental potential. While a gene regulatory network describing establishment of these cells has been generated, much remains to be learned about the dynamics of this process. Here, we use fluorescent in situ hybridization chain reaction to quantify the spatiotemporal dynamics of neural crest formation in Xenopus. We find that the initial onset of neural crest genes is broad and partially overlapping, with distinct anterior-posterior and medio-lateral biases. A shared neural crest domain emerges, but some genes retain relative expression differences that persist into migratory stages, producing stream-specific gene expression patterns. These differences correlate with dynamic expression of the neural plate border factors pax3 and zic1. Correlating relative intensities of pax3 and zic1 with the presence or absence of nascent neural crest transcripts predicts that these factors can differentially regulate snai2 and sox8, which we confirm experimentally. Strikingly, later stages display an inverse correlation between neural crest and neural plate border factors, suggesting that pax3 and zic1 initially promote neural crest gene activation but are downregulated as neural crest identity emerges. - Source: PubMed
Publication date: 2026/02/20
Montequin AndrewLaBonne Carole
MEP glia share molecular features with oligodendrocytes while maintaining a distinct hybrid signature.
Motor Exit Point (MEP) glia are spinal cord-derived glial cells that myelinate peripheral motor axons, bridging the central and peripheral nervous systems. They have a hybrid profile, sharing features with oligodendrocytes and Schwann cells. Yet, significant gaps remain in our understanding of complex MEP glial lineage and identity. MEP glia express neural tube and canonical oligodendrocyte lineage markers and , as well as the neural crest marker . Here, we show that the oligodendrocyte markers and are not expressed in MEP glia. These findings refine the molecular signature of MEP glia, enhancing their peripheral identity. - Source: PubMed
Publication date: 2026/01/21
Dallo Tessa CFontenas Laura
Advancing knock-in approaches for robust genome editing in zebrafish.
Precise genome editing remains a major challenge in functional genomics, particularly for generating knock-in (KI) alleles in model organisms. Here, we introduce the mini-golden system, a versatile Golden Gate-based subcloning platform that enables rapid assembly of donor constructs containing homology arms and a gene of interest. This system offers a library of middle entry vectors including diverse genes, enhancing the preparation of donor minicircles for KI applications. Using the mini-golden system, we efficiently generated a foxd3CreER KI zebrafish line, allowing conditional recombination in neural crest cells. To further improve genome editing precision, we developed a synthetic exon-based donor template strategy combined with fluorescence screening. Using this approach, we successfully engineered a targeted isoleucine-to-valine substitution (Ile-to-Val) in hbaa1.2, one of the two adult hemoglobin alpha genes in zebrafish. Importantly, despite the high sequence similarity between hbaa1.2 and its paralog hbaa1.1, our strategy specifically edited hbaa1.2, demonstrating the effectiveness of the synthetic exon approach. This method minimized undesired recombination and significantly improved the identification of lines carrying the edited genome. Together, we provide a robust toolkit for efficient and precise genome engineering in zebrafish, with broad applicability to other model systems. - Source: PubMed
Publication date: 2026/02/18
Rodriguez-Parks AnjelicaBeezley Ella GraceManna SteffaniSilaban IsabellaAlmutawa Sarah ICao SiyangAhmed HossamGuyer MeganBaker SeanRichards Mark PKang Junsu
The lncRNA SENCR of polymorphism rs12420823 drives breast cancer progression and its overexpression regulates this process via the miR-3648/FOXD3 axis.
The roles of long noncoding RNA SENCR (lncRNA SENCR) and its variant rs12420823 in triple-negative breast cancer (TNBC) susceptibility, progression, and molecular mechanisms remain unclear. thus, this study investigated the association of lncRNA SENCR and rs12420823 with TNBC risk and prognosis and explored the functional SENCR/miR-3648/FOXD3 axis. This study involving 205 TNBC patients and 203 controls, the rs12420823 polymorphism was genotyped and clinically correlated, revealing that the C allele is associated with reduced TNBC risk, while the TT genotype correlates with larger tumors, lymph node metastasis, advanced stage, and poorer survival. Prognosis was evaluated using Kaplan. The lncRNA SENCR and its variant rs12420823 play significant roles in TNBC Meier survival analysis and multivariate Cox regression. Through qRT-PCR analysis of serum and cell lines, lncRNA SENCR was found downregulated in TNBC, especially in TT genotype carriers. Mechanistic investigations, including luciferase reporter and RNA immunoprecipitation (RIP) assays, demonstrated that lncRNA SENCR directly binds to miR-3648, which targets FOXD3. Functional assays such as MTT and Transwell experiments showed that SENCR overexpression suppresses TNBC cell proliferation, migration, and invasion, effects reversed by a miR-3648 mimic. Furthermore, SENCR upregulates FOXD3 mRNA, an effect also abolished by miR-3648. In conclusion, the rs12420823 C allele confers protection against TNBC, and lncRNA SENCR acts as a tumor suppressor by sponging miR-3648 to regulate FOXD3, underscoring its prognostic and therapeutic relevance. - Source: PubMed
Publication date: 2026/01/07
Kong LingjunXue JiajieYang JiaqiChen JianxingMo Caiqin

AMH Gene anti-Mullerian hormone

Related genes to: AMH Gene anti-Mullerian hormone

Related products to: AMH Gene anti-Mullerian hormone

Related articles to: AMH Gene anti-Mullerian hormone

OTUB2/ALYREF axis modulates the docetaxel resistance of castration-resistant prostate cancer via upregulating ABCG4-mediated drug efflux.

Dynamic and non-uniform expression of key transcription factors provides insights into the emergence of neural crest cells at the neural plate border.

MEP glia share molecular features with oligodendrocytes while maintaining a distinct hybrid signature.

Advancing knock-in approaches for robust genome editing in zebrafish.

The lncRNA SENCR of polymorphism rs12420823 drives breast cancer progression and its overexpression regulates this process via the miR-3648/FOXD3 axis.