Tracking TrkA’s Trafficking: NGF Receptor Trafficking Controls NGF Receptor Signaling

Moises, T; Dreier, Agnieszka; Flohr, Stefanie; Esser, Marc; Brauers, Eva; Reiss, Kathleen; Merken, D.; Weis, Joachim; Krüttgen, Alex

doi:10.1007/s12035-007-8000-1

Cited by 28 publications

(16 citation statements)

References 95 publications

(109 reference statements)

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“…Understanding how DCAMKL1-mediated microtubule polymerization promotes the phosphorylation of Runx2 is an area of active investigation. It has been established that microtubules can facilitate signaling from the cell surface to the nucleus through retrograde transport of kinases (Moises et al, 2007). Therefore, stabilization of microtubules by DCAMKL1 within osteoblasts may facilitate the localization of certain kinases in the nucleus that promote Runx2 phosphorylation.…”

Section: Generation and Analysis Of Dcamkl1/runx2 Compound Mutant Micmentioning

confidence: 99%

The microtubule-associated protein DCAMKL1 regulates osteoblast function via repression of Runx2

Zou¹,

Greenblatt²,

Brady³

et al. 2013

J Cell Biol

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Section: Generation and Analysis Of Dcamkl1/runx2 Compound Mutant Micmentioning

confidence: 99%

The microtubule-associated protein DCAMKL1 regulates osteoblast function via repression of Runx2

Zou¹,

Greenblatt²,

Brady³

et al. 2013

J Cell Biol

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“…NGF binds to its TrkA receptor at the plasma membrane, leading to "transient" activation of the Ras-ERK signaling pathway and phosphoinositide 3 (PI3) -kinase, which promotes cell survival (Fig. 3) (Moises et al, 2007, Liu et al, 2007. Next, the NGF-TrkA complex is endocytosed and localized to early endosomes.…”

Section: Endosomes In Neurite Extensionmentioning

confidence: 99%

Organelles in developing neurons: essential regulators of neuronal morphogenesis and function

Sekine¹,

Miura²,

Chihara³

2009

Int. J. Dev. Biol.

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Eukaryotic cells contain multiple intracellular organelles which are structurally and functionally distinct membrane-delimited compartments. Organelles play vital roles in many cellular events in essentially all eukaryotic cells. Although the canonical roles of organelles are well described by classical in vitro studies, little is known about the specific physiological roles of organelles in neurons, which possess extremely polarized cellular structures and have a massive cellular volume compared with most eukaryotic cells. Studies that make use of recently developed genetic and microscopic techniques are currently elucidating the unexpectedly specialized roles of intracellular, membrane-delimited organelles in neuronal morphogenesis and function, and in human disease. Here we review recent advances in understanding the roles of organelles (the ERGolgi secretory pathway, endosomes and mitochondria) in developing neurons.

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“…37,38 Strong staining was seen in 30 (13%) tumors, moderate in 53 (23%), and weak in 70 (30%) samples, respectively. No NTRK1-pY674/ pY675 expression was detected in 82 (35%) tumors (Supplementary Table S2).…”

Section: Clinicopathological Parameters and Patient Outcomementioning

confidence: 99%

“…[30][31][32][33][34][35][36][37][38] The frequencies of expression intensities for NTRK1, NTRK1-pY674/ pY675, SHP-1, TP53, ER, HER2, PgR, and Ki-67 are summarized in Supplementary Table S2.…”

Section: Clinicopathological Parameters and Patient Outcomementioning

confidence: 99%

Phosphorylation of NTRK1 at Y674/Y675 induced by TP53-dependent repression of PTPN6 expression: A potential novel prognostic marker for breast cancer

Youssef¹,

Gillett

Agbaje

et al. 2014

Modern Pathology

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We have identified a ligand-independent mechanism whereby the tumor suppressor, TP53, induces nerve growth factor receptor, NTRK1, phosphorylation at Y674/Y675 (NTRK1-pY674/pY675), via the repression of the NTRK1-phosphatase, PTPN6. This results in suppression of breast cancer cell proliferation. In this investigation, we aimed to establish whether perturbation of the wild-type TP53-NTRK1-pY674/pY675-PTPN6 pathway has an impact on disease-free survival of breast cancer patients without neo-adjuvant treatment. A total of 308 tumor samples were stained for NTRK1, NTRK1-pY674/pY675, PTPN6, and TP53 expression. Association between expression levels and disease-free survival was determined by the univariate/multivariate and Kaplan-Meir methods of analysis. DNA from tumors was sequenced to identify mutant or wild-type TP53. Tumors expressing NTRK1-pY674/pY675 but with undetectable or low levels of PTPN6 and TP53 were associated with prolonged 5, 10, and 15 years' disease-free survival by 48%, 36%, and 37%, respectively, in the multivariate analysis (Po0.05). A similar result was observed in tumors expressing wild-type TP53, NTRK1-pY674/pY675, and low or undetectable levels of PTPN6. Given that estrogen receptor-positive breast cancers encode wild-type TP53, we analyzed this expression pattern in these tumors. Multivariate analysis showed that it was significantly and independently predictive of prolonged survival by 66%, 70%, and 84%, respectively, (Po0.05). The Kaplan-Meir method demonstrated that NTRK1-pY674/pY675 together with undetectable or low levels of PTPN6 correlated with 59% probability of disease-free survival (median survival 15 years), compared with 7% probability of disease-free survival (median survival 4.5 years) when absent. In luminal A tumors, the presence of this pattern was estimated to have a 61% probability of disease-free survival (median survival 15 years), compared with 6% probability of disease-free survival (median survival 3 years) when it was absent. These results strongly suggest that expression of NTRK1-pY674/pY675 together with wild-type TP53 and low levels of PTPN6 expression are predictors of improved disease-free survival and that they could be useful biomarkers to predict clinical outcome. Breast cancer is a leading cause of early mortality among women. 1 The incidence varies worldwide, with developed countries having higher rates than developing countries. 1,2 Although the rate of breast cancer has continued to increase, 3 mortality rates have decreased, partly due to the enhanced use of diagnostic and screening techniques. 4,5

show abstract

Tracking TrkA’s Trafficking: NGF Receptor Trafficking Controls NGF Receptor Signaling

Cited by 28 publications

References 95 publications

The microtubule-associated protein DCAMKL1 regulates osteoblast function via repression of Runx2

The microtubule-associated protein DCAMKL1 regulates osteoblast function via repression of Runx2

Organelles in developing neurons: essential regulators of neuronal morphogenesis and function

Phosphorylation of NTRK1 at Y674/Y675 induced by TP53-dependent repression of PTPN6 expression: A potential novel prognostic marker for breast cancer

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