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The downregulation of miR-199a contributes to paclitaxel (PTX) resistance in prostate cancer. YES1 mediates the regulation of miR-199a in prostate cancer PTX resistance.
findings identify acquired amplification of YES1 as a recurrent and targetable mechanism of resistance to EGFR inhibition in EGFR-mutant lung cancers and demonstrate the utility of transposon mutagenesis in discovering clinically relevant mechanisms of drug resistance.
Study on the role of miR-140-5p in inhibiting tumorigenesis in gastric cancer thru targeting YES proto-oncogene 1(YES1).
Our results suggest that H19 functions as a competitive endogenous RNA (ceRNA) by acting as a sink for miR-17-5p, revealing a potential ceRNA regulatory network involving H19 and miR-17-5p with a role in the modulation of YES1 expression
c-Yes plays an important role in migration and invasion of epithelial ovarian cancer.
Up-regulation of miR-210 inhibits hepatocellular carcinoma cell proliferation. Yes1 is a target of miR-210 and affects cell proliferation in HCC.
findings indicate that miR-203 induces the apoptosis of KB cells by directly targeting Yes-1, suggesting its application in anti-cancer therapeutics
Results demonstrate a unique role for Yes in phosphorylation of FAK and in promoting PCa metastasis. Therefore, phosphorylated FAK Y861 and increased Yes expression may be predictive markers for PCa metastasis.
results indicated that miR-17-5p might play a role in human ovarian cancer by up-regulating YES1 expression.
Increased YES/SFK activation might serve as a clinical biomarker for predicting tumor resistance to IGF-1R inhibition.
YES1 and YAP transcript levels were higher in liver metastases of patients with colon cancer after 5FU-based neoadjuvant chemotherapy.
YES kinase as a proximal glucose-specific signal in the Cdc42-signaling cascade.
we identified CRKL/YES as critical interrelated pathways necessary for rhabdomyosarcoma cell growth and survival and suggest a potential therapeutic role of SRC family kinase inhibition in the treatment of rhabdomyosarcoma.
Expression of HPV type 16 E7 resulted in increase in Src and Yes proteins level, but did not alter the level of Fyn.
Taken together, our findings demonstrate that Yes and Lyn phosphorylate EGFR at Y1101, which influences EGFR nuclear translocation in this model of cetuximab resistance.
study concludes that Yes is a central mediator for malignant mesothelioma cell growth that is not shared with other Src family kinases such as c-Src
c-Yes regulates specific oncogenic signalling pathways important for colon cancer progression that is not shared with c-Src.
Functional activation of Src family kinase yes protein is essential for the enhanced malignant properties of human melanoma cells expressing ganglioside GD3.
Yes-associated protein may play important roles in different pathways in distinct lung tumor subtypes.
c-Yes was expressed in malignant melanoma, and squamous cell carcinoma type skin neoplasms.
investigated signaling pathways in early development by comparison of the phosphoproteome of wild type embryos with Fyn/Yes knockdown embryos that display specific convergence and extension cell movement defects
Ganglioside GD3 enhances invasiveness of gliomas by forming a complex with PDGFRalpha and Yes Kinase.
serum also activates TEAD-dependent transcription in a time- and dose-dependent manner and we identify Inter-alpha-inhibitor (IalphaI) as a component in serum capable of activating the Yes/YAP/TEAD pathway
Differentiation of embryonic stem cells is driven by c-Src is antagonized by c-Yes.
The antiapoptotic effect of YES1 activation in response to testicular heat insult may mediate via the regulation of extracellular signal-regulated kinase (ERK)/metastasis-associated 1 (MTA1) cascade.
Results suggest that LKB1 inactivation in the context of RAS activation facilitates metastasis by inducing an SFK-dependent expansion of a prometastatic, CD24(+) tumor subpopulation.
YAP, TEAD2 and Yes are highly expressed in self-renewing embryonic stem cells, and are activated by LIF.
eIF4E and yes have cooperative roles in oncogenic transformation
Data show that in response to angiotensin II, the ability of ERK1/2 to remain within the cytoplasm or translocate into the nucleus is controlled by c-Src/Yes/Fyn or heterotrimeric G protein/PKCzeta signaling, respectively.
Data imply that distinct modes of spatial activation and membrane delivery, under the control of specific acylation attachment sequences and endosome sub-type requirements, define distinct properties of the three SFKs (Src family kinases).
Binding of CD95 Ligand to CD95 on glioblastoma cells recruit Yes and the p85 subunit of phosphatidylinositol 3-kinase to CD95, which signal invasion via the glycogen synthase kinase 3-beta pathway and subsequent expression of matrix metalloproteinases.
This gene is the cellular homolog of the Yamaguchi sarcoma virus oncogene. The encoded protein has tyrosine kinase activity and belongs to the src family of proteins. This gene lies in close proximity to thymidylate synthase gene on chromosome 18, and a corresponding pseudogene has been found on chromosome 22.
Yamaguchi sarcoma oncogene
, cellular yes-1 protein
, proto-oncogene c-Yes
, proto-oncogene tyrosine-protein kinase YES
, tyrosine-protein kinase Yes
, protein-tyrosine kinase
, tyrosine-protein kinase yes
, viral oncogene yes-1 homolog 1
, v-yes-1 Yamaguchi sarcoma viral oncogene homolog 1
, viral oncogene yes-1 homolog 1-like
, proto-oncogene tyrosine-protein kinase Yes-like
, proto-oncogene tyrosine-protein kinase Yes
, viral oncogene yes homolog
, c-yes proto-oncogene
, Yamagichi sarcoma viral (v-yes-1) oncogene homolog 1
, Yamaguchi sarcoma viral oncogene homolog 1