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Morphine significantly downregulated the expression of miRNA-219-5p, which targets WEE1 to suppress Tyr15 expressions and activate Cdc2, thus inhibiting the morphine-induced macrophage apoptosis.
Results revealed that WEE1 is indispensable for maintaining genomic stability and it functions as a haploinsufficient tumor suppressor.
Wee1 is directly or indirectly involved in the mechanism of the circadian rhythm-dependent changes in docetaxel-induced intestinal damage.
The induction of Wee1 under hypoxia was confirmed both at the mRNA and protein levels.
In this study, we found that the chromosomal wee1 gene is also down-regulated by KLF3.
The regulation of Wee1 by SadA and SadB kinases is essential for the differentiation of polarized neurons.
Mammalian Wee1 plays a critical role in maintaining genome integrity and is essential for embryonic survival at the pre-implantation stage of mouse development.
expression of wee1 was directly regulated by the molecular components of the circadian clockwork in the regenerating liver
transcription repressive activity of TBP-related factor 2 to wee1 promoter needs association with the promoter and TFIIA
the suppression of nuclear import of cyclin B1, the induction of Wee1 kinase activity, and the transient nuclear accumulation of p21(CIP1/WAF1) may play important roles in the transient cell cycle delay in response to ionizing radiation
downregulation of lncRNA NEAT1_2 radiosensitizes hepatocellular carcinoma cells through regulation of miR-101-3p/WEE1 axis
ATR inhibition synergizes with WEE1 inhibition in TNBC.
Inhibition of Wee1 by its specific inhibitor MK1775 in combination with sorafenib restored the KRAS mutated cells' response to the multi-target tyrosine kinase inhibitor.
miR-26b governed temozolomide (TMZ)-resistance-mediate epithelial-mesenchymal transition partly due to governing its target Wee1.
the data suggest the importance of WEE1 as an enabler of branching vascularisation in colorectal cancer liver metastases.
WEE1 is over-expressed and could enhance gastric cancer cell proliferation and metastasis
Wee1 is identified as a novel direct target of miR-194. Ectopic expression of Wee1 at least in part overcomes the suppressive impacts of miR-194 on the malignant phenotypes of human laryngeal squamous cell carcinoma
High WEE1 expression is associated with non-small cell lung cancer.
miR-503 could function as an enhancer of radiation responses in laryngeal carcinoma cells by inhibiting WEE1
Data suggest that SMURF1 is required for S phase progression; SMURF1 promotes ubiquitination-dependent degradation of WEE1; these functions of SMURF1 appear to be linked and may be important in cell proliferation and tumorigenesis. (SMURF1 = SMAD specific E3 ubiquitin protein ligase 1; WEE1 = wee 1 homolog [S pombe] protein)
Date show that when Wee1 alone is inhibited, Chk1 suppresses CDC45 loading and thereby limits the extent of unscheduled replication initiation and subsequent S-phase DNA damage, despite very high CDK-activity.
we overexpressed CKS1B in multiple cell lines and found increased sensitivity to PLK1 knockdown and PLK1 drug inhibition. Finally, combined inhibition of WEE1 and PLK1 results in less apoptosis than predicted based on an additive model of the individual inhibitors, showing an epistatic interaction and confirming a prediction of the yeast data.
Wee1 staining intensity was a predictor of favorable metastasis-free and overall survival compared to strong intensity and no or weak staining
These results highlight the key role of WEE1 suppression to combat glioblastomas. Moreover, it showed beneficial possibilities of WEE1 suppression with different anticancer approaches for neurological malignancies.
Wee1 inhibition potentiates Wip1-dependent tumor sensitization effect by reducing levels of Hipk2 kinase, a negative regulator of Wip1 pathway.
High nuclear expression of WEE1 protein is associated with all glioma grades and types.
Consistent with these findings, a genome-scale pooled RNA interference screen revealed that toxic doses of MK-1775 are suppressed by CDK2 or Cyclin A2 knockdown. These findings support G2 exit as the more significant effect of Wee1 inhibition in pancreatic cancers.
WEE1 is regulated at the translational level by CPEB1 and miR-15b in a coordinated and cell-cycle-dependent manner.
Data show that proto-oncogene protein Mdm2 inactivation successfully protects tumor suppressor protein (p53)-proficient cells against the cytotoxic effects of Wee1 protein inhibition.
nasopharyngeal carcinoma cells depend on CHK1 and WEE1 activity for growth
the identification of a second member of the RNase H2 complex, RNase H2B, being able to complement the root growth phenotype of WEE1(KO) plants, is reported.
mutant alleles of the genes encoding subunits of the ribonuclease H2 (RNase H2) complex, known for its role in removing ribonucleotides from DNA-RNA duplexes, were identified as suppressor mutants of WEE1 knockout plants.
The plant WEE1 kinase acquired an indirect developmental function that is important for meristem maintenance upon replication stress.
The WEE1 gene is not rate-limiting for cell cycle progression under normal growth conditions but is a critical target of the ATR-ATM signaling cascades that inhibit the cell cycle upon activation of the DNA integrity checkpoints.
This gene encodes a nuclear protein, which is a tyrosine kinase belonging to the Ser/Thr family of protein kinases. This protein catalyzes the inhibitory tyrosine phosphorylation of CDC2/cyclin B kinase, and appears to coordinate the transition between DNA replication and mitosis by protecting the nucleus from cytoplasmically activated CDC2 kinase.
WEE1 homolog (S. pombe)
, wee1-like protein kinase 2
, Wee1 kinase
, Wee1-like protein kinase
, wee1 tyrosine kinase
, wee1-like protein kinase
, wee1A kinase
, WEE1 tyrosine kinase
, WEE1+ homolog