threonine/cancer mamar

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A computational approach for investigating the mutational landscape of RAC-alpha serine/threonine-protein kinase (AKT1) and screening inhibitors against the oncogenic E17K mutation causing breast cancer.

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Breast cancer (BC) is the most commonly diagnosed cancer among females worldwide, and among the BC-associated mutations in various proteins, mutations in the RAC-alpha serine/threonine-protein kinase (AKT1) remain the most dominant. We thus attempted to understand the potential molecular

Phosphorylation of threonine residues on Shc promotes ligand binding and mediates crosstalk between MAPK and Akt pathways in breast cancer cells.

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Scaffold proteins play important roles in regulating signalling network fidelity, the absence of which is often the basis for diseases such as cancer. In the present work, we show that the prototypical scaffold protein Shc is phosphorylated by the extracellular signal-regulated kinase, Erk. In

Tyrosyl phosphorylated serine-threonine kinase PAK1 is a novel regulator of prolactin-dependent breast cancer cell motility and invasion.

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Despite efforts to discover the cellular pathways regulating breast cancer metastasis, little is known as to how prolactin (PRL) cooperates with extracellular environment and cytoskeletal proteins to regulate breast cancer cell motility and invasion. We implicated serine-threonine kinase

Phosphorylation of Sox2 at Threonine 116 is a Potential Marker to Identify a Subset of Breast Cancer Cells with High Tumorigenecity and Stem-Like Features.

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We have previously identified a novel phenotypic dichotomy in breast cancer (BC) based on the response to a SRR2 (Sox2 regulatory region 2) reporter, with reporter responsive (RR) cells being more tumorigenic/stem-like than reporter unresponsive (RU) cells. Since the expression level of Sox2 is

Use of a monoclonal antibody to detect elevated levels of a modified nucleoside, N-[9-(beta-D-ribofuranosyl)purin-6-ylcarbamoyl]-L-threonine, in the urine of breast cancer patients.

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Monoclonal antibodies to the modified nucleoside N-[9-(beta-D-ribofuranosyl)purin-6-ylcarbamoyl]-L-threonine (t6A) have been produced and characterized. These antibodies were utilized in a radioimmunoassay to quantitate the levels of this modified nucleoside in the urine of patients with benign

Combination of zoledronic acid and serine/threonine phosphatase inhibitors induces synergistic cytotoxicity and apoptosis in human breast cancer cells via inhibition of PI3K/Akt pathway.

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The aim of this study was to investigate the cytotoxic and apoptotic effects of zoledronic acid (ZA) in combination with serine/threonine protein phosphatase inhibitors, calyculin-A (CA) and okadaic acid (OA), in human MCF-7 and MDA-MB-231 breast cancer cells. XTT cell viability assay was used to

Alterations in the activity and expression of serine/threonine protein phosphatases during all trans retinoic acid-induced apoptosis in breast cancer cells.

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Retinoids exert different effects on malignant cells with various phenomena. They can induce differentiation and apoptosis in various cancer cells. However, the underlying mechanism of these effects is not clear. There are data related to the role of protein phosphatases during retinoid-induced

Reduced expression of the regulatory A subunit of serine/threonine protein phosphatase 2A in human breast cancer MCF-7 cells.

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The beta1 subunit of integrin is serine/threonine phosphorylated in growth arrested human breast cancer MCF-7 cells, while it is not in quiescent normal human breast epithelial (HBE) cells. Using the affinity-purified antibodies PB788-9 against the synthetic oligopeptide that contained

Histopathology and clinical assessment correlate with the cysteine-serine-valine-threonine-cysteine-glycine (CSVTCG) receptor of thrombospondin-1 in breast tumors.

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Thrombospondin-1 (TSP-1) is a matrix protein implicated in mechanisms of tumor metastasis. TSP-1 has a characteristic Cysteine-Serine-Valine-Threonine-Cysteine-Glycine (CSVTCG) sequence that functions as a tumor cell adhesion domain. Our laboratory has isolated a novel CSVTCG specific tumor cell

A putative serine/threonine kinase encoding gene BTAK on chromosome 20q13 is amplified and overexpressed in human breast cancer cell lines.

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DNA amplification on chromosome 20q13 is commonly detected in breast cancer and correlates with poor prognosis. Definitive critical target genes on this amplicon have however, not yet been identified. We describe in this paper isolation of a novel gene named BTAK, encoding a putative member of

MicroRNA‑299‑5p inhibits cell metastasis in breast cancer by directly targeting serine/threonine kinase 39.

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Numerous studies have demonstrated that microRNAs (miRNAs) play a key role in human carcinogenesis and metastasis. For example, miR‑299‑5p has previously been revealed to be dysregulated in several human cancers. However, the biological function of miR‑299‑5p in breast cancer remains unclear. The

The serine-threonine protein phosphatase PPM1D is frequently activated through amplification in aggressive primary breast tumours.

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The serine-threonine protein phosphatase PPM1D is likely to play an important role in tumorigenesis. Through inactivation of p38 MAPK, PPM1D acts as a negative feedback regulator of p53 tumour suppressor gene and controls the expression of other cell cycle regulatory proteins, such as CCND1. In

Eya3 promotes breast tumor-associated immune suppression via threonine phosphatase-mediated PD-L1 upregulation.

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Eya proteins are critical developmental regulators that are highly expressed in embryogenesis but downregulated after development. Amplification and/or re-expression of Eyas occurs in many tumor types. In breast cancer, Eyas regulate tumor progression by acting as transcriptional cofactors and

MicroRNA-215 acts as a tumor suppressor in breast cancer by targeting AKT serine/threonine kinase 1.

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There are accumulating reports that microRNAs are dysregulated in a number of human cancer types, and that they may function as tumor suppressors or oncogenes in tumorigenesis and tumor development. microRNA-215 (miR-215) has been identified as a tumor suppressor in epithelial ovarian, pancreatic,

Identification of NEK3 Kinase Threonine 165 as a Novel Regulatory Phosphorylation Site That Modulates Focal Adhesion Remodeling Necessary for Breast Cancer Cell Migration.

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Accumulating evidence supports a role for prolactin (PRL) in the development and progression of human breast cancer. Although PRL is an established chemoattractant for breast cancer cells, the precise molecular mechanisms of how PRL regulates breast cancer cell motility and invasion are not fully

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