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Profil bibliographique

Arisa Tanigawa

Informations fournies par OpenAlex. Research Africa ne déduit ni nationalité, ni poste, ni coordonnées personnelles.

3Publications signalées
54Citations signalées
1Affiliations récentes

Les institutions déclarées

Les domaines associés

Advanced biosensing and bioanalysis techniquesDevelopmental Biology and Gene RegulationCellular Mechanics and InteractionsPluripotent Stem Cells ResearchRNA Interference and Gene Delivery

Les publications récentes

Accès ouvert 2026 preprint OpenAlex

SOX2 terminates trophectoderm competence in inner cell mass by closing trophectoderm enhancers

Naoki Hirono, Masanori Uchikawa, Arisa Tanigawa, Takeru Fujii et autres

SUMMARY During embryonic development, cellular competence to respond to differentiation signals changes dynamically. Although the mechanisms underlying competence acquisition have been extensively studied, those underlying competence loss remain unclear. In preimplantation mouse embryos, Hippo signaling shifts from regulating trophectoderm (TE) fate specification …

gb, jp (code pays fourni par la source)

0 citations bioRxiv (Cold Spring Harbor Laboratory)
Accès ouvert 2022 article OpenAlex

A heterozygous LAMA5 variant may contribute to slowly progressive, vinculin-enhanced familial FSGS and pulmonary defects

Jun‐Ya Kaimori, Yamato Kikkawa, Daisuke Motooka, Tomoko Namba‐Hamano et autres

The LAMA5 gene encodes laminin α5, an indispensable component of glomerular basement membrane and other types of basement membrane. A homozygous pathological variant in LAMA5 is known to cause a systemic developmental syndrome including glomerulopathy. However, the roles of heterozygous LAMA5 gene …

jp, cn, us (code pays fourni par la source)

6 citations JCI Insight
Accès ouvert 2020 article OpenAlex

Combi-CRISPR: combination of NHEJ and HDR provides efficient and precise plasmid-based knock-ins in mice and rats

Kazuto Yoshimi, Yuichiro Oka, Yoshiki Miyasaka, Yuko Kotani et autres

CRISPR-Cas9 are widely used for gene targeting in mice and rats. The non-homologous end-joining (NHEJ) repair pathway, which is dominant in zygotes, efficiently induces insertion or deletion (indel) mutations as gene knockouts at targeted sites, whereas gene knock-ins (KIs) via homology-directed repair …

jp (code pays fourni par la source)

48 citations Human Genetics

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