FOXG1 (Forkhead Box G1)

Moreover, adolescent administration remained highly effective, rescuing myelination, axonal bundle thickness, and microglial activation. These findings identify neuronal FOXG1 as a master regulator of neuron-glia interactions and establish neuron-targeted AAV-FOXG1 as a potent and clinically translatable therapeutic strategy across diverse severities of FOXG1 syndrome.

Conversely, miR-101-mediated suppression of METTL3 disrupts EIF3J-AS1-FOXG1 binding, restoring MIF expression and promoting autophagy. These findings highlight EIF3J-AS1 and METTL3 as potential therapeutic targets, with disruption of EIF3J-AS1-FOXG1 interactions representing a novel autophagy-modulating strategy for glioma treatment.

This study demonstrates that FA supplementation alleviates gestational arsenic exposure-induced spatial learning and memory deficits, at least partially, by increasing SAM levels in the developing brain. Our findings identify potential targets and strategies for preventing cognitive impairments in offspring due to gestational arsenic exposure.

After targeting mechanosensory-restricted Foxg1, ampullary organs formed within neuromast lines, suggesting that Foxg1 normally represses their development, whether directly or indirectly. We speculate that electrosensory organs may be the 'default' developmental fate of lateral line primordia in electroreceptive vertebrates.

Therefore, loss of FOXG1 transitions the progenitor to a gliogenic state, producing either astrocytes or oligodendrocytes depending on FGF signalling levels. Our results uncover how FOXG1 integrates extrinsic signalling via the FGF pathway to regulate the sequential generation of neurons, astrocytes, and oligodendrocytes in the cerebral cortex.

Rigosertib, volasertib, and onvansertib showed equivalent efficacy to that of standard care agents (irinotecan and cisplatin) in vivo with significant growth inhibition superior to cisplatin in PDX models of platinum-sensitive and platinum-resistant SCLC. We established the efficacy of PLK1 inhibitors in vitro and in vivo using PDX models of platinum-sensitive and resistant relapsed SCLC. An ongoing phase II trial is currently testing the efficacy of onvansertib in patients with SCLC (NCT05450965).

This spatial expression pattern of SOX2 and FOXG1 proteins observed in immature teratoma mirrors the lineage differentiation and migration trajectories of primitive neuroepithelial components typically seen in embryonic neurogenesis and cortical development. In daily practice, the combined application of SOX2 and FOXG1 SOX2 and FOXG1 helps identify the primitive neuroepithelial components in immature teratoma, avoid misjudgment of similar morphologies, and thereby assist in the histological grading and clinical decision-making.

Consistently, Pak1 expression is upregulated by FOXG1 overexpression and downregulated upon FoxO6 loss in proliferative NSCs. These data suggest a pro-oncogenic role for FoxO6, downstream of GBM-associated elevated FOXG1, in controlling quiescence exit, and shed light on the potential functions of this underexplored FoxO family member.

S. tetrandra and its active compound coclaurine may serve as effective adjuvant therapies to improve cisplatin efficacy in the treatment of NSCLC.

Postnatal administration of Plp1-targeting antisense oligonucleotides (ASOs) in Foxg1 c946del mice improved neurological deficits. Our data suggest Plp1 as a new target for therapeutic strategies mitigating disease phenotypes in FOXG1 syndrome patients.

miR-105-5p promotes HDAC2 expression by reducing FOXG1, inhibits histone acetylation, and aggravates the malignant biological behavior of TNBC cells.

Foxg1a specifically regulates the development and regeneration of Islet1-labeled hair cells. These data suggest that Foxg1 may be a valuable target for investigation of clinical hair cell regeneration.