Physiology
Loss of autophagy impairs physiological steatosis by accumulation of NCoR1Autophagy regulates fatty acid and triglyceride synthesis at the transcriptional level by fine-tuning the levels of NCoR1, a negative regulator of nuclear receptors. Defective autophagy impairs physiological steatosis both under fasting conditions and after hepatectomy.
TMEM16A chloride channel does not drive mucus productionDespite being essential for airway hydration, TMEM16A is not required for mucus (MUC5AC) production. Cell proliferation is the main driver for TMEM16A up-regulation during inflammation.
Expression of a constitutively active human STING mutant in hematopoietic cells produces an Ifnar1-dependent vasculopathy in miceTransgenic expression of a mutant hSTING cDNA under the control of the Vav1 gene promoter leads to a vasculopathy similar to that of the interferonopathy, STING-associated vasculopathy of infancy.
m6A-mRNA methylation regulates cardiac gene expression and cellular growthThis study provides evidence that m6A methylation is dynamically regulated during human and murine cardiac disease and highlights an important role of the m6A methylase Mettl3 in regulating cardiac growth by gene expression control.
Substrate fluxes in brown adipocytes upon adrenergic stimulation and uncoupling protein 1 ablationQuantification of substrate fluxes in brown adipocytes clarifies contributors to extracellular acidification, identifies a futile cycle of lipolysis and re-esterification, and suggests a role for glycogen during activation.
Secretory granule protein chromogranin B (CHGB) forms an anion channel in membranesThe CHGB subfamily of secretory granule proteins forms a new family of anion-selective channels by interacting with membranes via two amphipathic α-helices. The channel exhibits higher anion selectivity, larger conductance, higher DIDS-binding affinity, and higher Cl− sensitivity than other known anion channels.
Multiple membrane extrusion sites drive megakaryocyte migration into bone marrow blood vesselsMegakaryocytes enter bone marrow sinusoids to generate platelets by extrusion of internal membrane into the plasma membrane at fusion sites rather than microtubule-driven proplatelet extension.