Last update 01 Nov 2024

NTRK x Fra-1

Last update 01 Nov 2024

Basic Info

Related Targets

NTRKFra-1

Drugs associated with NTRK x Fra-1

XP-103

Target

Fra-1 x NTRK

Mechanism

Fra-1 inhibitors [+1]

Active Org.

Xynomic Pharmaceuticals, Inc.

Originator Org.

Xynomic Pharmaceuticals, Inc.

Active Indication

Solid tumor

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with NTRK x Fra-1

100 Translational Medicine associated with NTRK x Fra-1

0 Patents (Medical) associated with NTRK x Fra-1

Literatures (Medical) associated with NTRK x Fra-1

01 Feb 2022·Journal of Cell ScienceQ2 · BIOLOGY

The nucleolar δ isoform of adapter protein SH2B1 enhances morphological complexity and function of cultured neurons

Q2 · BIOLOGY

Article

Author: Choudhury, Tahrim A. ; Argetsinger, Lawrence S. ; Vander, Paul B. ; Maures, Travis J. ; Kong, Seongbae ; Klaft, Olivia G. J. ; Doche, Michael E. ; Cote, Jessica L. ; Carter-Su, Christin ; Joe, Ray M. ; Svezhova, Nadezhda ; Ellis, Michael ; Cline, Joel M.

ABSTRACTThe adapter protein SH2B1 is recruited to neurotrophin receptors, including TrkB (also known as NTRK2), the receptor for brain-derived neurotrophic factor (BDNF). Herein, we demonstrate that the four alternatively spliced isoforms of SH2B1 (SH2B1α–SH2B1δ) are important determinants of neuronal architecture and neurotrophin-induced gene expression. Primary hippocampal neurons from Sh2b1−/− [knockout (KO)] mice exhibit decreased neurite complexity and length, and BDNF-induced expression of the synapse-related immediate early genes Egr1 and Arc. Reintroduction of each SH2B1 isoform into KO neurons increases neurite complexity; the brain-specific δ isoform also increases total neurite length. Human obesity-associated variants, when expressed in SH2B1δ, alter neurite complexity, suggesting that a decrease or increase in neurite branching may have deleterious effects that contribute to the severe childhood obesity and neurobehavioral abnormalities associated with these variants. Surprisingly, in contrast to SH2B1α, SH2B1β and SH2B1γ, which localize primarily in the cytoplasm and plasma membrane, SH2B1δ resides primarily in nucleoli. Some SH2B1δ is also present in the plasma membrane and nucleus. Nucleolar localization, driven by two highly basic regions unique to SH2B1δ, is required for SH2B1δ to maximally increase neurite complexity and BDNF-induced expression of Egr1, Arc and FosL1.

15 May 2019·Journal of Cell Science

Expression of Concern: Gene trap analysis of germ cell signaling to Sertoli cells: NGF-TrkA mediated induction of Fra1 and Fos by post-meiotic germ cells

Article

Author: Rassoulzadegan, M. ; Lopez-Fernandez, L. A. ; Ranc, F. ; Cuzin, F. ; Scimeca, J. C. ; Vidal, F. ; Lopez, P.

[This Expression of Concern relates to J. Cell Sci. (2001) 114, [435-443.][2]][2] Journal of Cell Science was alerted to duplicated HPRT blots in Fig. 4A and Fig. 7C of this paper. The authors state that the conclusions of the paper are not affected by the duplicated control blots, but were unable

01 Aug 2009·Journal of NeurosurgeryQ1 · MEDICINE

Candidate genes for sensitivity and resistance of human glioblastoma multiforme cell lines to erlotinib

Q1 · MEDICINE

Article

Author: Schmidt, Ursula ; Hielscher, Thomas ; Unterberg, Andreas ; Feuerhake, Friedrich ; Halatsch, Marc-Eric ; Vougioukas, Vassilios I. ; Löw, Sarah ; Mursch, Kay

ObjectThe authors have previously reported that erlotinib, an EGFR tyrosine kinase inhibitor, exerts widely variable antiproliferative effects on 9 human glioblastoma multiforme (GBM) cell lines in vitro and in vivo. These effects were independent of EGFR baseline expression levels, raising the possibility that more complex genetic properties form the molecular basis of the erlotinib-sensitive and erlotinib-resistant GBM phenotypes. The aim of the present study was to determine candidate genes for mediating the cellular response of human GBMs to erlotinib.MethodsComplementary RNA obtained in cell lines selected to represent the sensitive, somewhat responsive, and resistant phenotypes were hybridized to CodeLink Human Whole Genome Bioarrays.ResultsExpression analysis of 814 prospectively selected genes involved in major proliferation and apoptosis signaling pathways identified 19 genes whose expression significantly correlated with phenotype. Functional annotation analysis revealed that 2 genes (DUSP4 and STAT1) were significantly associated with sensitivity to erlotinib, and 10 genes (CACNG4, FGFR4, HSPA1B, HSPB1, NFATC1, NTRK1, RAC1, SMO, TCF7L1, and TGFB3) were associated with resistance to erlotinib. Moreover, 5 genes (BDNF, CARD6, FOSL1, HSPA9B, and MYC) involved in antiapoptotic pathways were unexpectedly found to be associated with sensitivity. Gene expressions were confirmed by quantitative polymerase chain reaction.ConclusionsBased on an analysis of gene expressions in cell lines with sensitive, somewhat responsive, and resistant phenotypes, the authors propose candidate genes for GBM response to erlotinib. The 10 gene candidates for conferring GBM resistance to erlotinib may represent therapeutic targets for enhancing the efficacy of erlotinib against GBMs. Five additional genes warrant further investigation into their role as putative cotargets of erlotinib.

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