| CREB3L1 deficiency impairs odontoblastic differentiation and molar dentin deposition partially through the TMEM30B. | CREB3L1 deficiency impairs odontoblastic differentiation and molar dentin deposition partially through the TMEM30B.
Li Y, Lin Y, Guo J, Huang D, Zuo H, Zhang H, Yuan G, Liu H, Chen Z., Free PMC Article | 10/10/2024 |
| Transcription factor old astrocyte specifically induced substance is a novel regulator of kidney fibrosis. | Transcription factor old astrocyte specifically induced substance is a novel regulator of kidney fibrosis.
Yamamoto A, Morioki H, Nakae T, Miyake Y, Harada T, Noda S, Mitsuoka S, Matsumoto K, Tomimatsu M, Kanemoto S, Tanaka S, Maeda M, Conway SJ, Imaizumi K, Fujio Y, Obana M., Free PMC Article | 06/26/2021 |
| The endoplasmic reticulum stress transducer old astrocyte specifically induced substance (OASIS) positively regulates glial scar formation in spinal cord injury (SCI). OASIS deletion inhibited the development of N-cadherin-positive reactive astrocytes that form glial scars and promoted axon growth and functional recovery after SCI. | The endoplasmic reticulum stress transducer old astrocyte specifically induced substance positively regulates glial scar formation in spinal cord injury.
Sumida Y, Kamei N, Suga N, Ochi M, Adachi N., Free PMC Article | 02/16/2019 |
| The results suggest that CREB3L1 is required for decidualization in mice and humans and may be linked to the pathogenesis of endometriosis in a progesterone-dependent manner. | cAMP-Response Element-Binding 3-Like Protein 1 (CREB3L1) is Required for Decidualization and its Expression is Decreased in Women with Endometriosis.
Ahn JI, Yoo JY, Kim TH, Kim YI, Ferguson SD, Fazleabas AT, Young SL, Lessey BA, Ahn JY, Lim JM, Jeong JW., Free PMC Article | 12/17/2016 |
| OASIS affects the expression of HIF-1alpha target genes through the protein interaction with HIF-1alpha, and that OASIS-HIF-1alpha complexes may play essential roles in angiogenesis during bone development. | OASIS modulates hypoxia pathway activity to regulate bone angiogenesis.
Cui M, Kanemoto S, Cui X, Kaneko M, Asada R, Matsuhisa K, Tanimoto K, Yoshimoto Y, Shukunami C, Imaizumi K., Free PMC Article | 09/10/2016 |
| Higher levels of CREB3L1 protein are correlated with increased doxorubicin sensitivity of xenograft RCC tumors | Identification of CREB3L1 as a Biomarker Predicting Doxorubicin Treatment Outcome.
Denard B, Pavia-Jimenez A, Chen W, Williams NS, Naina H, Collins R, Brugarolas J, Ye J., Free PMC Article | 04/9/2016 |
| Increased susceptibility to dextran sulfate sodium-induced colitis in the endoplasmic reticulum stress transducer OASIS deficient mice. | Increased susceptibility to dextran sulfate sodium-induced colitis in the endoplasmic reticulum stress transducer OASIS deficient mice.
Hino K, Saito A, Asada R, Kanemoto S, Imaizumi K., Free PMC Article | 10/25/2014 |
| We conclude that OASIS functions as an anti-regenerative transcription factor by establishing a non-permissive microenvironment to regenerating axons | OASIS regulates chondroitin 6-O-sulfotransferase 1 gene transcription in the injured adult mouse cerebral cortex.
Okuda H, Tatsumi K, Horii-Hayashi N, Morita S, Okuda-Yamamoto A, Imaizumi K, Wanaka A. | 10/18/2014 |
| Temporally regulates the differentiation from neural precursor cells into astrocytes [review] | Physiological functions of endoplasmic reticulum stress transducer OASIS in central nervous system.
Saito A., Free PMC Article | 07/19/2014 |
| Fbxw7 controls osteogenesis and chondrogenesis by targeting OASIS and BBF2H7, respectively, for degradation. | F-box and WD repeat domain-containing-7 (Fbxw7) protein targets endoplasmic reticulum-anchored osteogenic and chondrogenic transcriptional factors for degradation.
Yumimoto K, Matsumoto M, Onoyama I, Imaizumi K, Nakayama KI., Free PMC Article | 12/7/2013 |
| Gliosis-specific transcription factor OASIS coincides with proteoglycan core protein genes in the glial scar and inhibits neurite outgrowth. | Gliosis-specific transcription factor OASIS coincides with proteoglycan core protein genes in the glial scar and inhibits neurite outgrowth.
Iseki K, Hagino S, Nikaido T, Zhang Y, Mori T, Yokoya S, Hozumi Y, Goto K, Wanaka A, Tase C. | 06/8/2013 |
| Findings demonstrate a novel mechanism by which OASIS and its associated family members are modulated by the unfolded protein response to finely control astrocyte differentiation. | Unfolded protein response, activated by OASIS family transcription factors, promotes astrocyte differentiation.
Saito A, Kanemoto S, Kawasaki N, Asada R, Iwamoto H, Oki M, Miyagi H, Izumi S, Sanosaka T, Nakashima K, Imaizumi K. | 11/3/2012 |
| OASIS plays crucial roles in promoting the differentiation of early goblet cells to mature goblet cells in the large intestine. | The endoplasmic reticulum stress transducer OASIS is involved in the terminal differentiation of goblet cells in the large intestine.
Asada R, Saito A, Kawasaki N, Kanemoto S, Iwamoto H, Oki M, Miyagi H, Izumi S, Imaizumi K., Free PMC Article | 05/5/2012 |
| OASIS may play a role in bone formation through the expression of type I collagen and the secretion of bone matrix proteins in fracture healing. | Roles of the endoplasmic reticulum stress transducer OASIS in fracture healing.
Funamoto T, Sekimoto T, Murakami T, Kurogi S, Imaizumi K, Chosa E. | 12/24/2011 |
| OASIS regulates skeletal development by osteoblast-dependent and -independent mechanisms. | Distinct mechanisms are responsible for osteopenia and growth retardation in OASIS-deficient mice.
Murakami T, Hino S, Nishimura R, Yoneda T, Wanaka A, Imaizumi K. | 05/28/2011 |
| OASIS-/- mice exhibit severe osteopenia involving a decrease in type I collagen in the bone matrix and a dysfunction of osteoblasts, which show abnormal expansion of the rough ER. | Effects of the bisphosphonate risedronate on osteopenia in OASIS-deficient mice.
Sekiya H, Murakami T, Saito A, Hino S, Tsumagari K, Ochiai K, Imaizumi K. | 09/27/2010 |
| Signalling mediated by the endoplasmic reticulum stress inducer Oasis is involved in bone formation. | Signalling mediated by the endoplasmic reticulum stress transducer OASIS is involved in bone formation.
Murakami T, Saito A, Hino S, Kondo S, Kanemoto S, Chihara K, Sekiya H, Tsumagari K, Ochiai K, Yoshinaga K, Saitoh M, Nishimura R, Yoneda T, Kou I, Furuichi T, Ikegawa S, Ikawa M, Okabe M, Wanaka A, Imaizumi K. | 01/21/2010 |
| OASIS expressed in astrocytes plays important roles in protection against kainic acid-induced damage to hippocampal pyramidal neurons. | Increased vulnerability of hippocampal pyramidal neurons to the toxicity of kainic acid in OASIS-deficient mice.
Chihara K, Saito A, Murakami T, Hino S, Aoki Y, Sekiya H, Aikawa Y, Wanaka A, Imaizumi K. | 01/21/2010 |
| In mice, the OASIS gene may be related to proteoglycan expression and play a role in the differentiation of the odontoblast and cells in inner enamel epithelium. | Comparison of expression patterns between CREB family transcription factor OASIS and proteoglycan core protein genes during murine tooth development.
Hikake T, Mori T, Iseki K, Hagino S, Zhang Y, Takagi H, Yokoya S, Wanaka A. | 01/21/2010 |
| Oasis is an endoplasmic reticulum stress transducer in astrocytes, a membrane-bound transcription factor that activates genes in the stress response. | Cleavage of the membrane-bound transcription factor OASIS in response to endoplasmic reticulum stress.
Murakami T, Kondo S, Ogata M, Kanemoto S, Saito A, Wanaka A, Imaizumi K. | 01/21/2010 |
| Our results reveal pivotal roles for OASIS in modulating the unfolded protein response in astrocytes, and the possibility that cell type-specific UPR signalling also exists in other cells | OASIS, a CREB/ATF-family member, modulates UPR signalling in astrocytes.
Kondo S, Murakami T, Tatsumi K, Ogata M, Kanemoto S, Otori K, Iseki K, Wanaka A, Imaizumi K. | 01/21/2010 |
| Data suggest that OASIS protein positively regulates gene transcription in a subset of reactive astrocytes, and may influence the reaction of injured central nervous system tissues [OASIS protein]. | Expression of OASIS, a CREB/ATF family transcription factor, in CNS lesion and its transcriptional activity.
Nikaido T, Iseki K, Mori T, Takaki H, Yokoya S, Hagino S, Takeda J, Zhang Y, Takeuchi M, Kikuchi S, Wanaka A. | 01/21/2010 |