| Regulation of microtubule nucleation in mouse bone marrow-derived mast cells by ARF GTPase-activating protein GIT2. | Regulation of microtubule nucleation in mouse bone marrow-derived mast cells by ARF GTPase-activating protein GIT2.
Sulimenko V, Sládková V, Sulimenko T, Dráberová E, Vosecká V, Dráberová L, Skalli O, Dráber P., Free PMC Article | 03/21/2024 |
| A similar number of both total and gender-unique transcripts were significantly altered in response to GIT2 heterozygosity in early life-stage (2 month-old) mice | Multidimensional informatic deconvolution defines gender-specific roles of hypothalamic GIT2 in aging trajectories.
van Gastel J, Cai H, Cong WN, Chadwick W, Daimon C, Leysen H, Hendrickx JO, De Schepper R, Vangenechten L, Van Turnhout J, Verswyvel J, Becker KG, Zhang Y, Lehrmann E, Wood WH 3rd, Martin B, Maudsley S. | 06/27/2020 |
| GIT2(-/-) mice present a prematurely distorted thymic structure and dysfunction compared to age-matched 12 month-old wild-type control (C57BL/6) mice. | Genomic deletion of GIT2 induces a premature age-related thymic dysfunction and systemic immune system disruption.
Siddiqui S, Lustig A, Carter A, Sankar M, Daimon CM, Premont RT, Etienne H, van Gastel J, Azmi A, Janssens J, Becker KG, Zhang Y, Wood W, Lehrmann E, Martin JG, Martin B, Taub DD, Maudsley S., Free PMC Article | 11/18/2017 |
| GIT2 plays an important role in MRE11/ATM/H2AX-mediated DNA damage responses. | Nuclear GIT2 is an ATM substrate and promotes DNA repair.
Lu D, Cai H, Park SS, Siddiqui S, Premont RT, Schmalzigaug R, Paramasivam M, Seidman M, Bodogai I, Biragyn A, Daimon CM, Martin B, Maudsley S., Free PMC Article | 05/30/2015 |
| GIT2 is an essential terminator of TLR signaling and loss of GIT2 leads to uncontrolled inflammation and severe organ damage | The GTPase-activating protein GIT2 protects against colitis by negatively regulating Toll-like receptor signaling.
Wei J, Wei C, Wang M, Qiu X, Li Y, Yuan Y, Jin C, Leng L, Wang J, Yang X, He F., Free PMC Article | 09/13/2014 |
| these findings underscore the importance of the cytoskeleton in both osteoblast and osteoclast function and demonstrate that GIT2 plays essential roles in skeletal metabolism, affecting both bone formation and bone resorption in vivo. | The cytoskeletal regulatory scaffold protein GIT2 modulates mesenchymal stem cell differentiation and osteoblastogenesis.
Wang X, Liao S, Nelson ER, Schmalzigaug R, Spurney RF, Guilak F, Premont RT, Gesty-Palmer D., Free PMC Article | 12/22/2012 |
| GIT2 has a key role in regulating the chemokine-mediated motility of double-positive thymocytes | Regulation of thymocyte positive selection and motility by GIT2.
Phee H, Dzhagalov I, Mollenauer M, Wang Y, Irvine DJ, Robey E, Weiss A., Free PMC Article | 06/14/2010 |
| Results suggest that paxillin-kinase-linker is an integral component of growth factor and cell adhesion cross-talk signaling, controlling the development of front-rear cell polarity and directional cell migration. | Paxillin-kinase-linker tyrosine phosphorylation regulates directional cell migration.
Yu JA, Deakin NO, Turner CE., Free PMC Article | 02/15/2010 |
| Hence, GIT2-KO mice display anxiety-like behavior in an absence of depressive-like responses. | Anxiety-like behaviors in mice lacking GIT2.
Schmalzigaug R, Rodriguiz RM, Phillips LE, Davidson CE, Wetsel WC, Premont RT., Free PMC Article | 01/21/2010 |
| Analysis of endogenous GIT expression revealed a nearly ubiquitous distribution of GIT2, whereas GIT1 is restricted to specific cell types even in tissues with apparently high GIT1 expression and is entirely absent from some tissues. | Differential expression of the ARF GAP genes GIT1 and GIT2 in mouse tissues.
Schmalzigaug R, Phee H, Davidson CE, Weiss A, Premont RT. | 01/21/2010 |
| GIT2 links chemotaxis and superoxide production in neutrophils.Loss of GIT2 in vivo leads to an immunodeficient state. | Neutrophil direction sensing and superoxide production linked by the GTPase-activating protein GIT2.
Mazaki Y, Hashimoto S, Tsujimura T, Morishige M, Hashimoto A, Aritake K, Yamada A, Nam JM, Kiyonari H, Nakao K, Sabe H. | 01/21/2010 |