| Macrophage GIT1 promotes oligodendrocyte precursor cell differentiation and remyelination after spinal cord injury. | Macrophage GIT1 promotes oligodendrocyte precursor cell differentiation and remyelination after spinal cord injury.
Liu H, Yi J, Zhang C, Li Y, Wang Q, Wang S, Dai S, Zheng Z, Jiang T, Gao P, Xue A, Huang Z, Kong F, Wang Y, He B, Guo X, Li Q, Chen J, Yin G, Zhao S. | 08/20/2024 |
| Git1-PGK1 interaction achieves self-protection against spinal cord ischemia-reperfusion injury by modulating Keap1/Nrf2 signaling. | Git1-PGK1 interaction achieves self-protection against spinal cord ischemia-reperfusion injury by modulating Keap1/Nrf2 signaling.
Xu T, Gao P, Huang Y, Wu M, Yi J, Zhou Z, Zhao X, Jiang T, Liu H, Qin T, Yang Z, Wang X, Bao T, Chen J, Zhao S, Yin G., Free PMC Article | 05/28/2023 |
| Brain-specific deletion of GIT1 impairs cognition and alters phosphorylation of synaptic protein networks implicated in schizophrenia susceptibility. | Brain-specific deletion of GIT1 impairs cognition and alters phosphorylation of synaptic protein networks implicated in schizophrenia susceptibility.
Fass DM, Lewis MC, Ahmad R, Szucs MJ, Zhang Q, Fleishman M, Wang D, Kim MJ, Biag J, Carr SA, Scolnick EM, Premont RT, Haggarty SJ., Free PMC Article | 12/3/2022 |
| GIT1 is an untolerized autoantigen involved in immunologic disturbance of spermatogenesis. | GIT1 is an untolerized autoantigen involved in immunologic disturbance of spermatogenesis.
Nagahori K, Kuramasu M, Kawata S, Yakura T, Li Z, Hirai S, Qu N, Itoh M. | 04/16/2022 |
| GIT1 protects traumatically injured spinal cord by prompting microvascular endothelial cells to clear myelin debris. | GIT1 protects traumatically injured spinal cord by prompting microvascular endothelial cells to clear myelin debris.
Wan B, Li C, Wang M, Kong F, Ding Q, Zhang C, Liu H, Qian D, Deng W, Chen J, Tang P, Wang Q, Zhao S, Zhou Z, Xu T, Huang Y, Gu J, Fan J, Yin G., Free PMC Article | 07/31/2021 |
| Macrophage GIT1 Contributes to Bone Regeneration by Regulating Inflammatory Responses in an ERK/NRF2-Dependent Way. | Macrophage GIT1 Contributes to Bone Regeneration by Regulating Inflammatory Responses in an ERK/NRF2-Dependent Way.
Zhao SJ, Liu H, Chen J, Qian DF, Kong FQ, Jie J, Yin GY, Li QQ, Fan J., Free PMC Article | 06/19/2021 |
| The protective effort of GPCR kinase 2-interacting protein-1 in neurons via promoting Beclin1-Parkin induced mitophagy at the early stage of spinal cord ischemia-reperfusion injury. | The protective effort of GPCR kinase 2-interacting protein-1 in neurons via promoting Beclin1-Parkin induced mitophagy at the early stage of spinal cord ischemia-reperfusion injury.
Huang YF, Gu CJ, Wang Q, Xu L, Chen J, Zhou W, Zhou Z, Zhao SJ, Li LW, Kong FQ, Qian DF, Zhao X, Fan J, Li QQ, Yin GY. | 10/3/2020 |
| GIT/PIX Condensates Are Modular and Ideal for Distinct Compartmentalized Cell Signaling. | GIT/PIX Condensates Are Modular and Ideal for Distinct Compartmentalized Cell Signaling.
Zhu J, Zhou Q, Xia Y, Lin L, Li J, Peng M, Zhang R, Zhang M. | 09/26/2020 |
| These results collectively suggest that GIT1 is a critical participant in formation of the CD31(hi)Emcn(hi) vessel subtype, highlighting a novel biologic function of this scaffold protein in preosteoclasts. | GIT1 is critical for formation of the CD31(hi)Emcn(hi) vessel subtype in coupling osteogenesis with angiogenesis via modulating preosteoclasts secretion of PDGF-BB.
Xu T, Luo Y, Kong F, Lv B, Zhao S, Chen J, Liu W, Cheng L, Zhou Z, Zhou Z, Huang Y, Li L, Zhao X, Qian D, Fan J, Yin G. | 07/4/2020 |
| GIT1 interacted with Beclin1 and promoted Beclin1 phosphorylation at Thr119, which induced the disruption of Beclin1 and Bcl2 binding under starvation conditions, thereby, positively regulating autophagy. Taken together, the findings suggest a previously unappreciated role of GIT1 in autophagy of OCs during fracture repair | GIT1 contributes to autophagy in osteoclast through disruption of the binding of Beclin1 and Bcl2 under starvation condition.
Zhao SJ, Kong FQ, Cai W, Xu T, Zhou ZM, Wang ZB, Xu AD, Yang YQ, Chen J, Tang PY, Wang Q, Cheng L, Luo YJ, Zhou Z, Li LW, Huang YF, Zhao X, Yin GY, Xue MX, Fan J., Free PMC Article | 12/14/2019 |
| Our findings suggest that GIT1 significantly extenuates the sFlt-1-induced preeclampsia phenotypes by inhibiting eNOS activity, indicating a crucial role of GIT1 in the progression of preeclampsia. | Deletion of GIT1 Impacts eNOS Activity To Aggravate sFlt-1-Induced Preeclampsia Phenotype in Mice.
Zhang S, Zou C, Zhang Q., Free PMC Article | 01/19/2019 |
| Results provide evidence that loss of GIT1 alone is insufficient to drive a robust ADHD phenotype in distinct strains of mice. In contrast, multiple learning and memory defects have been observed using distinct GIT1-knockout lines, consistent with a predominant intellectual disability phenotype related to altered synaptic structural plasticity. | GIT1 regulates synaptic structural plasticity underlying learning.
Martyn AC, Toth K, Schmalzigaug R, Hedrick NG, Rodriguiz RM, Yasuda R, Wetsel WC, Premont RT., Free PMC Article | 06/30/2018 |
| GIT1 gene deletion can inhibit chondrocyte proliferation and apoptosis during the recovery of tibial plateau fracture, so as to delay chondrocyte differentiation and tibial plateau fracture healing. | GIT1 gene deletion delays chondrocyte differentiation and healing of tibial plateau fracture through suppressing proliferation and apoptosis of chondrocyte.
Chen P, Gu WL, Gong MZ, Wang J, Li DQ., Free PMC Article | 04/28/2018 |
| In astrocytes and neural stem cells, we identified G-protein-coupled receptor kinase-interacting protein 1 (GIT1) as a novel mTOR-binding protein, creating a unique mTOR complex lacking Raptor and Rictor | Proteomic analysis reveals GIT1 as a novel mTOR complex component critical for mediating astrocyte survival.
Smithson LJ, Gutmann DH., Free PMC Article | 05/13/2017 |
| studies indicated that GIT1 promotes metastasis of NSCLC cells. GIT1 was found to stimulate migration/invasion by altering the activity of Rac1/Cdc42 in NSCLC cells. | GIT1 promotes lung cancer cell metastasis through modulating Rac1/Cdc42 activity and is associated with poor prognosis.
Chang JS, Su CY, Yu WH, Lee WJ, Liu YP, Lai TC, Jan YH, Yang YF, Shen CN, Shew JY, Lu J, Yang CJ, Huang MS, Lu PJ, Lin YF, Kuo ML, Hua KT, Hsiao M., Free PMC Article | 10/29/2016 |
| This study demonstrated that the Presynaptic Deletion of GIT Proteins Results in Increased Synaptic Strength at a Mammalian Central Synapse. | Presynaptic Deletion of GIT Proteins Results in Increased Synaptic Strength at a Mammalian Central Synapse.
Montesinos MS, Dong W, Goff K, Das B, Guerrero-Given D, Schmalzigaug R, Premont RT, Satterfield R, Kamasawa N, Young SM Jr., Free PMC Article | 03/26/2016 |
| Results suggested that cyclic phosphorylation-dephosphorylation at Tyr- 554 of Git1 was crucial for dynamic interactions between Git1 and paxillin/Hic-5 in order to ensure coordinated cell motility. | Specific dephosphorylation at tyr-554 of git1 by ptprz promotes its association with paxillin and hic-5.
Fujikawa A, Matsumoto M, Kuboyama K, Suzuki R, Noda M., Free PMC Article | 01/23/2016 |
| It provides for the first time, to our knowledge, a possible mechanism for the concerted action of tyrosine kinases, GIT1/betaPIX proteins, and Ca(2+) in the propagation of signals leading to the regulation of microtubule nucleation in activated mast cells. | Microtubule nucleation in mouse bone marrow-derived mast cells is regulated by the concerted action of GIT1/βPIX proteins and calcium.
Sulimenko V, Hájková Z, Černohorská M, Sulimenko T, Sládková V, Dráberová L, Vinopal S, Dráberová E, Dráber P. | 07/25/2015 |
| results indicate that GIT1 regulates Smad1/5/8 phosphorylation and mediates BMP2 regulation of Runx2 expression, thus affecting endochondral ossification at the fracture site. | Decreased BMP2 signal in GIT1 knockout mice slows bone healing.
Sheu TJ, Zhou W, Fan J, Zhou H, Zuscik MJ, Xie C, Yin G, Berk BC., Free PMC Article | 07/4/2015 |
| Plateletderived growth factor inhibits osteoblast apoptosis through upregulating GIT1 expression. | Platelet‑derived growth factor promotes osteoblast proliferation by activating G‑protein‑coupled receptor kinase interactor‑1.
Wu Y, Zhang Y, Yin Q, Xia H, Wang J. | 05/16/2015 |
| GIT1 is an important signaling participant in fracture healing, with gene ablation leading to reduced callus vascularity and reduced osteoclast number in the healing callus. | Impaired angiogenesis during fracture healing in GPCR kinase 2 interacting protein-1 (GIT1) knock out mice.
Yin G, Sheu TJ, Menon P, Pang J, Ho HC, Shi S, Xie C, Smolock E, Yan C, Zuscik MJ, Berk BC., Free PMC Article | 01/17/2015 |
| GIT1-cortactin association through GIT1-Spa homology domain is required for cortactin localization to the leading edge and is essential for endothelial cell directional migration and tumor angiogenesis. | G-protein-coupled receptor-2-interacting protein-1 is required for endothelial cell directional migration and tumor angiogenesis via cortactin-dependent lamellipodia formation.
Majumder S, Sowden MP, Gerber SA, Thomas T, Christie CK, Mohan A, Yin G, Lord EM, Berk BC, Pang J., Free PMC Article | 03/22/2014 |
| GIT1 is a novel mediator of vascular remodeling by regulating vascular smooth muscle cell proliferation, migration, and apoptosis through phospholipase Cgamma and extracellular signal-regulated kinase 1/2 signaling pathways. | G-protein-coupled receptor kinase interacting protein-1 mediates intima formation by regulating vascular smooth muscle proliferation, apoptosis, and migration.
Pang J, Xu X, Wang X, Majumder S, Wang J, Korshunov VA, Berk BC., Free PMC Article | 06/15/2013 |
| novel roles for Cat-1 and its interactions with the Arf GTPases and paxillin in oncogenic transformation. | The adaptor protein and Arf GTPase-activating protein Cat-1/Git-1 is required for cellular transformation.
Yoo SM, Antonyak MA, Cerione RA., Free PMC Article | 11/24/2012 |
| Phosphorylation of tyrosine 321 of GIT1 is necessary for PDGF-induced association with FAK, FAK activation in focal adhesions, and for osteoblastic cell migration. | Phosphorylation of GIT1 tyrosine 321 is required for association with FAK at focal adhesions and for PDGF-activated migration of osteoblasts.
Ren Y, Yu L, Fan J, Rui Z, Hua Z, Zhang Z, Zhang N, Yin G. | 08/25/2012 |