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Preview: Nature Medicine - Issue - science feeds

Nature Medicine - Issue - science feeds

Nature Medicine is the premier journal for biomedical research. Respected internationally for the quality of its papers on areas ranging from infectious disease to cancer and neurodegeneration, Nature Medicine aims to bridge the gap between basic research


Science over speed




Autoimmune T cell recognition of alternative-reading-frame-encoded peptides


A recent study shows that a self-peptide generated in pancreatic islet beta cells through the translation of a noncanonical alternative reading frame in human insulin mRNA is recognized by both CD4+ and CD8+ T cells in type 1 diabetes.

A mouse recapitulating APOL1-associated kidney disease


In a recent study, researchers generated a mouse model expressing variant APOL1 that recapitulates human kidney disease. Variant APOL1 leads to caspase-1-dependent pyroptosis, which opens the door for the development of new druggable targets to treat APOL1-mediated kidney disease.

Untangling the role of mutant histone H3 in diffuse intrinsic pontine glioma


New studies advance the mechanistic understanding of mutant histone H3 in diffuse intrinsic pontine glioma (DIPG) and demonstrate two epigenetic approaches, BET inhibition and EZH2 inhibition, as potential therapeutic strategies for DIPG.

Refining strategies to translate genome editing to the clinic


In this Review, Cathomen and colleagues present the latest advances, including improvements in nuclease specificity and delivery, that will expedite the clinical translation of genome editing.

Glucocorticoid hormone-induced chromatin remodeling enhances human hematopoietic stem cell homing and engraftment


Glucocorticoid treatment of human cord blood hematopoietic stem cells increases expression of the receptor CXCR4 by chromatin remodeling, thereby enhancing hematopoietic stem cell homing and engraftment.

Transgenic expression of human APOL1 risk variants in podocytes induces kidney disease in mice


Risk variants of APOL1 associated with human chronic kidney disease have been identified, but causality has been unclear. Transgenic expression in mice now shows that such alleles can indeed cause renal disease.

Targeting CASP8 and FADD-like apoptosis regulator ameliorates nonalcoholic steatohepatitis in mice and nonhuman primates


Targeting CFLAR in mouse and non-human primates ameliorates non-alcoholic steatohepatitis by decreasing JNK signaling in hepatocytes.

Gpr124 is essential for blood–brain barrier integrity in central nervous system disease


The G-protein-coupled receptor GPR124, acting through the canonical Wnt pathway, is required for the maintenance of blood–brain barrier function in mouse models of stroke and glioblastoma.

A subset of platinum-containing chemotherapeutic agents kills cells by inducing ribosome biogenesis stress


Whereas cisplatin and carboplatin kill cancer cells by inducing DNA damage, another platinum derivative, oxaliplatin, induces cell death by triggering ribosome biogenesis stress.

Targeting c-FOS and DUSP1 abrogates intrinsic resistance to tyrosine-kinase inhibitor therapy in BCR-ABL-induced leukemia


The intrinsic resistance of BCR-ABL-expressing chronic myeloid leukemia stem cells to treatment with tyrosine-kinase inhibitors requires growth-factor signaling through the proteins c-Fos and DUSP1. Combined inhibition of BCR-ABL, c-Fos, and DUSP1 eradicated leukemia in vivo, pointing to a new therapeutic strategy for kinase-driven leukemias.

EZH2 is a potential therapeutic target for H3K27M-mutant pediatric gliomas


Although mutant H3K27M histones inhibit PRC2 in diffuse intrinsic pontine gliomas, these tumors exhibit significant amounts of PRC2 activity. The repression of several genes, including INK4A, by residual EZH2 activity is required for tumor growth, and EZH2 inhibitors therefore represent potential therapies for these patients.

Therapeutic targeting of polycomb and BET bromodomain proteins in diffuse intrinsic pontine gliomas


Nucleosomes containing mutant K27M histones in diffuse intrinsic pediatric gliomas (DIPG) exclude PRC2 binding and recruit BET bromodomain proteins; however, residual PRC2-dependent repression of specific loci, is required for DIPG oncogenesis. These results provide a rationale for targeting these epigenetic regulators in patients.

Autoimmunity against a defective ribosomal insulin gene product in type 1 diabetes


Use of an alternative open reading frame, potentially as a result of cellular stress, drives production of an unconventional insulin epitope that is recognized by cytotoxic T cells from individuals with type 1 diabetes; these T cells kill beta cells in vitro.

Deficiency of the hepatokine selenoprotein P increases responsiveness to exercise in mice through upregulation of reactive oxygen species and AMP-activated protein kinase in muscle


Selenoprotein P is released from the liver and acts through LRP1 in the muscle to contribute to exercise resistance in mouse and man by inhibiting ROS levels via inhibition of AMPK and PGC-1α.

HRDetect is a predictor of BRCA1 and BRCA2 deficiency based on mutational signatures


HRDetect represents a model integrating whole-genome sequencing mutation signatures associated with BRCA1 and BRCA2 deficiency. The implementation of this predictor across different tumor types identifies a larger proportion of patients displaying ‘BRCAness’ than previously recognized; they might derive benefit from platinum and PARP-inhibitor therapies.