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these data indicate that activation of autophagy reduces expression of STMN1 and p53, and the migration and invasion of cancer cells contributes to the anti-cancer effects of the Halofuginone. These findings may provide new insight into breast cancer prevention and therapy.
Low expression of STMN1 was found in 43.62%, and high expression of STMN1 was found in 56.38% of cases of osteosarcoma. High tumor expression of STMN1 was a prognostic marker for poor prognosis, poor response to chemotherapy, the presence of metastases, advanced Enneking surgical stage and the chondroblastic osteosarcoma subtype. The expression STMN1 was identified as an independent prognostic biomarker of osteosarcoma .
a transcription-independent mechanism for Stat3-mediated centrosome clustering that involves Stathmin, a Stat3 interactor involved in microtubule depolymerization, and the mitotic kinase PLK1, is reported.
Results suggest that stathmin is essential in bipolar spindle formation to maintain genomic stability during mitosis, and the depletion of stathmin prevents the initiation of chromosome instability by inducing senescence in human normal fibroblasts.
Results showed that STMN1 overexpression was significantly associated with lymphatic metastatic recurrence in pN0 esophageal squamous cell carcinoma (ESCC) patients. STMN1 levels are regulated by the PI3K pathway, and STMN1 can act as a surrogate marker of PI3K pathway signaling related to tumor recurrence.
The investigation confirmed that stathmin expression was correlated with more aggressive behavior of cervical cancer.
High STMN1 Expression is Associated with Cancer Progression and Chemo-Resistance in Lung Squamous Cell Carcinoma.
STMN1 expression was significantly associated with prognosis and tumour differentiation in ESCC, indicating that STMN1 expression is an independent prognostic factor for ESCC and could be a potential biomarker. Regulating the expression of STMN1 could influence tumour cell motility, invasion and proliferation
T3-mediated suppression of STMN1 supports the theory that T3 plays an inhibitory role in HCC tumor growth, and suggests that the lack of normal THR function leads to elevated STMN1 expression and malignant growth
These results suggest that stathmin acts as an oncogene and is transcriptionally regulated by mutant p53, but not by wild-type p53. Stathmin could be a potential anti-tumor therapeutic target in oral squamous cell carcinoma
Results suggest that Stathmin 1 (STMN1) plays an important role in cell proliferation and migration.
STMN1 expression was higher in basal-type cell lines than in luminal-type cell lines, and overall survival and post-progression survival in the high STMN1 expression breast cancer patients were shorter than in low STMN1 expression patients. High STMN1 expression is a possible marker of breast cancer aggressiveness in association with proliferation, phenotype and cancer stem cell type
we found upregulated expression of STMN1 in the atypical/anaplastic meningioma group, relative to that in the benign meningioma group. STMN1, therefore, is a promising target to improve cure rates in meningioma cases.
An increased risk of sporadic atypical meningioma recurrence can be found in cases with elevated expression of STMN1.
The miR-34a/STMN1/betaIII-tubulin axis maintains the microtubule cytoskeleton in osteosarcoma, and combining miR-34a with microtubule inhibitors can be investigated as a novel therapeutic strategy.
These findings suggest that Cdc2 is positively associatd with the development of taxol resistance. The Cdc2 inhibitor, purvalanol A, enhanced the cytotoxic effects of taxol through Op18/stathmin.
these results showed that stathmin expression was significantly up-regulated in LAC, which may act as a biomarker for LAC. Furthermore, silence of stathmin inhibiting LAC cell growth indicated that stathmin may be a promising molecular target for LAC therapy.
Increased stathmin correlated with pathologic grade, lymphatic invasion, advanced stage and poor survival of non-small cell lung cancer (NSCLC), which indicated that stathmin could serve as a potential biomarker of NSCLC
Results showed that patients with cancer displayed a higher stathmin expression than those of non-cancer individuals, and overexpression of stathmin correlated with tumor cell differentiation, lymph node invasion and high TNM stage. [review]
High STMN1 Expression Is Associated with Tumor Differentiation and Metastasis in Pancreatic Cancer.
STMN1 is a PDGFRalpha phospho-regulated target; its mis-regulation confers sensitivity to vinblastine cytotoxicity in glioblastoma
These findings suggest that during embryo implantation, knockdown of Stmn1 suppresses decidualisation by inhibiting the expression of p-Akt, HIF-1alpha and VEGF, thus leading to impaired embryo implantation.
The data suggest that STMN1 mediates the progesterone production by modulating the promoter activity of Star and Cyp11a1.
EGFR suppression of mitotic regulators including Rcc2 and Stathmin 1 are a mechanism for catagen induction in mouse skin
We identified stathmin as a key molecule aiding in septin-independent cytokinesis, demonstrated that stathmin supplementation is sufficient to override cytokinesis failure in SEPT7-null fibroblasts
Overexpressing stathmin reduces complement receptor 3-mediated phagocytosis and cellular activation, implicating a pivotal inhibitory role for stathmin in classically activated macrophages.
Stathmin cooperates with p27(kip1) to control the early phase of G1 to S phase transition and that this function may be of particular relevance in the context of tumor progression.
The protein profiles during murine embryo implantation were clarified. Stathmin 1 might be a potential regulator of embryo implantation.
Results show an important role for stathmin during adult neurogenesis in the subgranular zone of the mouse hippocampus; propose that stathmin controls the transition from neuronal precursors to early postmitotic neurons
Stathmin mutations disrupt changes in microtubule stability, GluA2 localization, synaptic plasticity and memory.
Stmn deletion does not prolong the lifespan of spinal muscular atrophy-like mice, suggesting that stathmin dysregulation and microtubule disruption are not a cause but rather a consequence of SMA pathology.
stathmin expression is dispensable for tumor onset, at least in mice, thus making stathmin a virtually exclusive marker of aggressive disease and a promising therapeutic target for advanced cancers.
results demonstrate the mechanism of stathmin-dependent control of MT dynamics, Rho signaling, and permeability
Stathmin phosphorylates the microtubule network during T cell activation, resulting in increased microtubule growth rate dependent on the presence of stathmin.
GRPR and stathmin control in opposite directions both cued fear extinction and neural activities of the amygdala and prefrontal cortex
Stathmin, which alters microtubule dynamics, plays an essential role in maintenance of postnatal bone mass by regulating both osteoblast and osteoclast functions in bone.
These results provide evidence that stathmin-1 expression in uNK cells at the maternal-fetal interface may help modulate uterine natural killer cell function and may be beneficial for a successful pregnancy.
JNK1, JNK2 and c-Jun inhibit fibroblast proliferation by negatively regulating the levels of stathmin.
Aberrant stathmin levels may play a detrimental role in spinal muscular atrophy.
results suggest that up-regulation of stathmin1 in the dentate gyrus, secondary to PACAP deficiency, may create abnormal neuronal circuits that cause abnormal behavior
Op18 reveals the contribution of nonkinetochore microtubules to the dynamic organization of the vertebrate meiotic spindle.
This gene belongs to the stathmin family of genes. It encodes a ubiquitous cytosolic phosphoprotein proposed to function as an intracellular relay integrating regulatory signals of the cellular environment. The encoded protein is involved in the regulation of the microtubule filament system by destabilizing microtubules. It prevents assembly and promotes disassembly of microtubules. Multiple transcript variants encoding different isoforms have been found for this gene.
leukemia-associated phosphoprotein p18
, oncoprotein 18
, phosphoprotein 19
, phosphoprotein p19
, stathmin 1/oncoprotein 18
, transmembrane protein C1orf215
, leukemia associated phosphoprotein p18
, leukemia-associated gene protein
, leukemia-associated cytosolic phosphoprotein stathmin
, stathmin 1 a
, stathmin 1/oncoprotein 18b
, stathmin 1
, stathmin 1 b
, stathmin 1b
, stathmin clone XO35