Amit Kumar
National Institutes of Health
24 Papers
195 Citations
Amit Kumar is an academic researcher from National Institutes of Health. The author has contributed to research in topics: NODAL & Nodal signaling. The author has an hindex of 15, co-authored 24 publications. Previous affiliations of Amit Kumar include Johns Hopkins University & University of Arkansas for Medical Sciences.
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Papers
Cysteines and Disulfide Bonds as Structure-Forming Units: Insights From Different Domains of Life and the Potential for Characterization by NMR.
TL;DR: The impact of cysteine and disulfide bonds in the proteasome from different domains of life are presented and a condensed overview of recent NMR applications for the characterization of disulfides-bond containing biomolecules including advantages and limitations of the different approaches are given.
Nodal signaling recruits the histone demethylase Jmjd3 to counteract polycomb-mediated repression at target genes
TL;DR: A key function of the developmentally essential Nodal-Smads2/3 (Smad2 and Smad3) signaling pathway is to recruit the histone demethylase Jmjd3 to target genes, thereby counteracting repression by Polycomb, and suggests how transcriptional plasticity can arise through cooperation between the epigenetic machinery and developmental signaling pathways.
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Insulin inhibits the activation of transcription by a C-terminal fragment of the forkhead transcription factor FKHR: a mechanism for insulin inhibition of insulin-like growth factor binding protein-1 transcription.
TL;DR: Results suggest that insulin- and phosphatidylinositol-3 kinase-dependent phosphorylation of another site in the fragment by a kinase different from PKB/Akt inhibits transcription activation by the fragment.
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Critical role of p42/44(MAPK) activation in anisomycin and hepatocyte growth factor-induced LDL receptor expression: activation of Raf-1/Mek-1/p42/44(MAPK) cascade alone is sufficient to induce LDL receptor expression.
TL;DR: Dhawan et al. as mentioned in this paper showed that although exposure to anisomycin resulted in rapid and strong activation of p46/54JNK and p38MAPK, with a delayed low level dual-phosphorylation of mitogen/extracellular protein kinase (p42/44MAPK), low density lipoprotein (LDL) receptor induction depends solely on the mild activation of the p42/ 44MAPK signaling cascade in HepG2 cells.
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Nodal signaling from the visceral endoderm is required to maintain Nodal gene expression in the epiblast and drive DVE/AVE migration.
Amit Kumar,Margaret Lualdi,George T. Lyozin,Prashant Sharma,Jadranka Loncarek,Xin-Yuan Fu,Michael R. Kuehn +6 more
TL;DR: A required role for VE Nodal to maintain normal levels of expression in the epiblast is supported, and signaling from both VE and epiblasts is suggested to be important for DVE/AVE migration.
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