Abstract.Structural, sedimentological, magnetostratigraphic, and nøAr/39Ar thermochronological investigations were conducted in the southern Chinese Tian Shan. On the basis of our own mapping and earlier investigations in the area, the Late Cenozoic southern Tian Shan thrust belt may be divided into four segments based on their style of deformation. From west to east, they are (1) Kashi-Aksu imbricate thrust system, (2) the Baicheng-Kuche fold and thrust system, (3) the Korla right-slip transfer system, and (

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A palaeomagnetic pole position, derived from a precisely dated primary remanence, with minimal uncertainties due to secular variation and structural correction, has been obtained for China’s largest dyke swarm, which trends for about 1000 km in a NNW direction across the North China craton. Positive palaeomagnetic contact tests on two dykes signify that the remanent magnetization is primary and formed during initial cooling of the intrusions. The age of one of these dykes, based on U–Pb dating of primary zircon, is 1769.1 ± 2.5 Ma. The mean palaeomagnetic direction for 19 dykes, after structural correction, is D = 36°, I = − 5°, k = 63, α95 = 4°, yielding a palaeomagnetic pole at Plat=36°N, Plong=247°E, dp = 2°, dm = 4° and a palaeolatitude of 2.6°S. Comparison of this pole position with others of similar age from the Canadian Shield allows a continental reconstruction that is compatible with a more or less unchanged configuration of Laurentia, Siberia and the North China craton since about 1800 Ma

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Annexin-A1 (ANXA1) has recently been proposed to play a role in microglial activation after brain ischemia, but the underlying mechanism remains poorly understood. Here, we demonstrated that ANXA1 is modified by SUMOylation, and SUMOylated ANXA1 could promote the beneficial phenotype polarization of microglia. Mechanistically, SUMOylated ANXA1 suppressed nuclear factor κB activation and the production of proinflammatory mediators. Further study revealed that SUMOylated ANXA1 targeted the IκB kinase (IKK) complex and selectively enhanced IKKα degradation. Simultaneously, we detected that SUMOylated ANXA1 facilitated the interaction between IKKα and NBR1 to promote IKKα degradation through selective autophagy. Further work revealed that the overexpression of SUMOylated ANXA1 in microglia/macrophages resulted in marked improvement in neurological function in a mouse model of cerebral ischemia. Collectively, our study demonstrates a previously unidentified mechanism whereby SUMOylated ANXA1 regulates microglial polarization and strongly indicates that up-regulation of ANXA1 SUMOylation in microglia may provide therapeutic benefits for cerebral ischemia.