PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 34314061-8 2021 VGLL4 knockdown attenuated CNH-induced PH and pulmonary artery remodeling by blunting signal transducer and activator of transcription 3 (STAT3) signaling; conversely, VGLL4 overexpression exacerbated the development of PH. 1-hydroxy-11-norcadinan-5-en-4-one 27-30 vestigial like family member 4 Mus musculus 0-5 34314061-9 2021 CNH enhanced the acetylation of VGLL4 and increased the interaction of ac-H3K9/VGLL4 and ac-H3K9/STAT3 in the lung tissues, and levels of ac-H3K9, p-STAT3/STAT3, and proliferation-associated protein levels were markedly up-regulated, whereas apoptosis-related protein levels were significantly downregulated, in the lung tissues of mice with CNH-induced PH. 1-hydroxy-11-norcadinan-5-en-4-one 0-3 vestigial like family member 4 Mus musculus 32-37 34314061-9 2021 CNH enhanced the acetylation of VGLL4 and increased the interaction of ac-H3K9/VGLL4 and ac-H3K9/STAT3 in the lung tissues, and levels of ac-H3K9, p-STAT3/STAT3, and proliferation-associated protein levels were markedly up-regulated, whereas apoptosis-related protein levels were significantly downregulated, in the lung tissues of mice with CNH-induced PH. 1-hydroxy-11-norcadinan-5-en-4-one 0-3 vestigial like family member 4 Mus musculus 79-84 34314061-9 2021 CNH enhanced the acetylation of VGLL4 and increased the interaction of ac-H3K9/VGLL4 and ac-H3K9/STAT3 in the lung tissues, and levels of ac-H3K9, p-STAT3/STAT3, and proliferation-associated protein levels were markedly up-regulated, whereas apoptosis-related protein levels were significantly downregulated, in the lung tissues of mice with CNH-induced PH. 1-hydroxy-11-norcadinan-5-en-4-one 342-345 vestigial like family member 4 Mus musculus 32-37 34314061-9 2021 CNH enhanced the acetylation of VGLL4 and increased the interaction of ac-H3K9/VGLL4 and ac-H3K9/STAT3 in the lung tissues, and levels of ac-H3K9, p-STAT3/STAT3, and proliferation-associated protein levels were markedly up-regulated, whereas apoptosis-related protein levels were significantly downregulated, in the lung tissues of mice with CNH-induced PH. 1-hydroxy-11-norcadinan-5-en-4-one 342-345 vestigial like family member 4 Mus musculus 79-84 34314061-10 2021 Notably, abrogation of VGLL4 acetylation reversed CNH-induced PH and pulmonary artery remodeling and suppressed STAT3 signaling. 1-hydroxy-11-norcadinan-5-en-4-one 50-53 vestigial like family member 4 Mus musculus 23-28 34314061-12 2021 In conclusion, VGLL4 acetylation upregulation could contribute to CNH-induced PH and pulmonary artery remodeling via STAT3 signaling, and abrogation of VGLL4 acetylation reversed CNH-induced PH. 1-hydroxy-11-norcadinan-5-en-4-one 66-69 vestigial like family member 4 Mus musculus 15-20 34314061-12 2021 In conclusion, VGLL4 acetylation upregulation could contribute to CNH-induced PH and pulmonary artery remodeling via STAT3 signaling, and abrogation of VGLL4 acetylation reversed CNH-induced PH. 1-hydroxy-11-norcadinan-5-en-4-one 179-182 vestigial like family member 4 Mus musculus 15-20 34314061-12 2021 In conclusion, VGLL4 acetylation upregulation could contribute to CNH-induced PH and pulmonary artery remodeling via STAT3 signaling, and abrogation of VGLL4 acetylation reversed CNH-induced PH. 1-hydroxy-11-norcadinan-5-en-4-one 179-182 vestigial like family member 4 Mus musculus 152-157 34314061-13 2021 Pharmacological or genetic deletion of VGLL4 might be a potential target for therapeutic interventions in CNH-induced PH. 1-hydroxy-11-norcadinan-5-en-4-one 106-109 vestigial like family member 4 Mus musculus 39-44