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Data show that the locomotion and blebbing of the primordial germ cells (PGCs) required F-actin, myosin II activity and RhoA/Rho-associated protein kinase (ROCK) signaling.
Data demonstrate a direct relationship between SHP-2(N308D) and ROCK activation in the developing heart.
Morphogenesis of the primitive gut tube is generated by Rho/ROCK/myosin II-mediated endoderm rearrangements.
The findings of the present study indicate that miR-142-3p plays a critical role in hematopoiesis, cardiogenesis, and somitegenesis in the early stage of mesoderm formation via regulation of Rock2a.
Double knockdown of rock2a disrupted interkinetic nuclear migration in the retina.
Data show that Rock2 acts as a negative regulator of the TGFbeta signaling pathway.
Study shows Increased apical and basal dendritic length and intersections were observed in rho-associated protein kinases 1 (ROCK1 +/-) but not rho-associated protein kinases 2 (ROCK2 +/-) mice. Observations implicate ROCK1 as a novel regulatory factor of neuronal dendritic structure and detail distinct and complementary roles of ROCKs in medial prefrontal cortex dendritic spine structure.
ROCK2 plays a critical role in inducing mucosal T cell activation and inflammatory responses in colitis
by differentially affecting CyPA and Bsg expressions, ROCK1 protects and ROCK2 jeopardizes the heart from pressure-overload heart failure with postcapillary pulmonary hypertension, for which celastrol may be a promising agent.
Data indicate that Rho-associated protein kinase (ROCK)-dependent intermittent T cell migration regulates tissue-sampling during acute lung injury.
A specific inhibitor of ROCK, Y-27632, was used to examine the role of ROCK in mouse colitis models. ROCK1 and ROCK2 were silenced respectively using RNA interference in Caco-2 cells. The expression of tight junction proteins and the downstream molecules of ROCK were assessed
that platelet ROCK2 plays important role in platelet function and thrombosis, but does not contribute to the pathogenesis of atherosclerosis and vascular remodeling
This study showed that , APC/C(Cdh1)-mediated degradation of Rock2 maintains the dendritic network, memory formation, and neuronal survival, suggesting that pharmacological inhibition of aberrantly accumulated Rock2 may be a suitable therapeutic strategy against neurodegeneration.
data suggest that activation of ROCK2 in adipose tissue contributes to obesity-induced insulin resistance; this may result in part from suppression of PPARgamma expression, leading to adipocyte hypertrophy and an increase in inflammatory cytokine production; ROCK2 may be a suitable target to improve insulin sensitivity in obesity
ROCK2 contributes to allergic airways responses likely via effects within ASM cells and within non-lymphocyte cells involved in lymphocyte activation and migration into the airways.
BRAF and ROKalpha form independent RAF1 complexes in embryonic fibroblasts (MEFs) treated with epidermal growth factor (EGF).
Dexamethasone up-regulates ROCK1/2 activity promoting migration, invasion and metastasis of melanoma cells.
these data suggest that ROCK2 signaling plays a critical role in controlling the development of TFH cells induced by autoimmune conditions through reciprocal regulation of STAT3 and STAT5 activation.
Data indicate that oxidative stress in diabetes causes a decrease in miR-133a expression leading to an increase in RhoA/Rho kinase pathway and muscle contraction.
Results strongly support the hypothesis that spinal RhoA/ROCK2 signaling plays a central role in the neuropathic pain. In addition, simvastatin might exert its antihyperalgesic and antiallodynic effects through the attenuation of sensitization of spinal nociceptive transmission that is modulated by mechanisms dependent on the RhoA/ROCK2 signaling.
p21-associated inhibition of early-stage malignant progression and the intense expression in papilloma outgrowths, identifies a novel, significant antagonism between p21 and ras(Ha)/ROCK2/NF-kappaB signalling in skin carcinogenesis.these data show that ROCK2 activation induces malignancy in ras(Ha)-initiated/promoted papillomas in the context of p53 loss and novel NF-kappaB expression
The effect of Smad4 was at least partially mediated by the downstream effectors Syk and ROCK2 transcription in megakaryocytes.
Here we describe the generation of a gene-targeted mouse line that enables CRE-inducible expression of a conditionally-active fusion between the ROCK2 kinase domain and the hormone-binding domain of a mutated estrogen receptor (ROCK2:ER). This two-stage system of regulation allows for tissue-selective expression of the ROCK2:ER fusion protein, which then requires administration of estrogen analogues
The results of the present study verify that ROCKII participates in the loss of DA neurons induced by MPTP and suggest that ROCKII inhibition may be a promising therapeutic target for PD.
These results indicate that tensile force induces in vivo gene expression associated with vascularization early in tensile-force-induced sutural bone formation. Moreover, the early induction of Vegf gene expression is regulated by CTGF and ROCK2.
While the loss of either Rock1 or Rock2 had no negative impact on tumorigenesis in mouse models of non-small cell lung cancer and melanoma, loss of both blocked tumor formation, as no tumors arise in which both Rock1 and Rock2 have been genetically deleted.
this study demonstrated that the levels of ROCK2 activity were significantly upregulated in peripheral blood mononuclear cells and inflamed mucosa from inflammatory bowel disease patients, and that ROCK2 activity in intestinal mucosa was positively correlated with disease severity
Taken together, Lin28A regulated the biological behaviors in Ovarian cancer cells through ROCK2 and the interaction of Lin28A/ROCK2 may be a new target for diagnosis and gene therapy of Ovarian cancer .
High RICK2 expression is associated with ovarian Cancer.
ROCK-dependent phosphorylation of NUP62 regulates p63 nuclear transport and squamous cell carcinoma proliferation.
ROCK2 is a target of miR-455-3p.
miR130a is a regulator of ROCK2 and can inhibit proliferation, migration and invasive ability of hepatocellular carcinoma cells, at least in part, by suppressing the expression of ROCK2.
Upregulation of ROCK2 was associated with the progression of breast cancer.
ROCK2 participates in cell adhesion by regulating ICAM-1 expression and the co-localization of adhesion molecules with vimentin.
qPCR demonstrated that melatonin downregulated ROCK2 gene expression, and upregulated the expression of the ZO1 and occludin genes. The levels of ZO1 and occludin localized in the tight junctions were markedly increased in the immunofluorescence assay.
This study showed that ROCK2 expression significantly increased in clinical gastric cancer tissues compared with adjacent non-cancer tissues.
The findings indicate that upregulation of the RhoA/ROCK pathway is significantly associated with cardiac hypertrophy-related Ca2+ dysregulation and suggest that ROCK inhibition prevents hypertrophic heart failure.
RhoA is activated in tumors from neuroblastoma patients, and elevated expression of Rho-associated kinase (ROCK)2 is associated with poor patient survival. Pharmacological or genetic inhibition of ROCK1 and 2, key molecules in Rho signaling, resulted in neuroblastoma cell differentiation and inhibition of neuroblastoma cell growth, migration, and invasion.
ROCK1 and ROCK2 contribute to the genetic susceptibility of hypertension and stroke.
these data indicate that ROCK proteins are overexpressed in diverse vascular tumors and suggest that specific targeting of ROCK2 proteins may show efficacy against malignant vascular tumors.
Fasudil exhibited protective effects on smoke exposure induced cognitive deficits which might involve with the regulation of Rho/ROCK/NF-kappaB pathways.
The increase in protein expression of ROCK2 in astrocytes and microglia suggests an important role for ROCK2 in glial Parkinson disease pathology, which is initiated already in normal aging.
ROCK2 protein level was inversely correlated with miR-101 level in NSCLC tissue samples.
RhoE and ROCK2 regulate chemoresistance in hepatocellular carcinoma.
Combined EGFR and ROCK inhibition effectively blocks proliferation of triple-negative breast cancer (TNBC) cells.
Inhibition of ROCK signaling restored polarity, decreased disorganization of F-actin, and led to reduction of proliferation of breast cancer cells.
Results indicate that ROCK1 and ROCK2 may exert different biological functions during the regulation of compaction and in ensuring development of porcine preimplantation embryos to the blastocyst stage.
ROCK2 plays a pivotal role in generating the intrinsic circadian rhythm of vascular contractility by receiving a cue from RORalpha.
It is highly possible that Rho-kinase plays an important role in the pathogenesis of in-stent restenosis. Rho-kinase is not involved in endothelial regeneration after vascular injury.
Rho-kinase analysis of coiled-coil association of the RhoA-binding domain
RhoA/Rho-kinase pathway is an important component of TGF-beta-induced effects on endothelial myosin light chain phosphorylation, cytoskeletal reorganization, and barrier integrity.
nucleus-localized ROCK2 targets p300 for phosphorylation to regulate its acetyltransferase activity
The protein encoded by this gene is a serine/threonine kinase that regulates cytokinesis, smooth muscle contraction, the formation of actin stress fibers and focal adhesions, and the activation of the c-fos serum response element. This protein, which is an isozyme of ROCK1 is a target for the small GTPase Rho.
Rho-associated kinase alpha
, rho-associated protein kinase 2
, rho-associated, coiled-coil containing protein kinase 2
, Rho-associated, coiled-coil containing protein kinase 2
, rho-associated protein kinase 2-like
, Rho-associated coiled-coil forming kinage 2
, p164 ROCK-2
, rho-associated, coiled-coil-containing protein kinase 2
, rho-associated, coiled-coil-containing protein kinase II
, Rho-associated coiled-coil forming kinase 2
, RhoA - binding serine/threosine kinase alpha (ROK - alpha)
, p150 ROK-alpha
, rhoA-binding kinase 2
, Rho-kinase alpha