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Purified anti-mouse CD68 antibody

RRID:AB_2044003

Antibody ID

AB_2044003

Target Antigen

CD68 See NCBI gene mouse

Proper Citation

(BioLegend Cat# 137001, RRID:AB_2044003)

Clonality

monoclonal antibody

Comments

Applications: ICFC, FC, IP, WB, IHC

Clone ID

Clone FA-11

Host Organism

rat

Vendor

BioLegend Go To Vendor

Cat Num

137001

Publications that use this research resource

The Microglial Innate Immune Receptor TREM2 Is Required for Synapse Elimination and Normal Brain Connectivity.

  • Filipello F
  • Immunity
  • 2018 May 15

Literature context:


Abstract:

The triggering receptor expressed on myeloid cells 2 (TREM2) is a microglial innate immune receptor associated with a lethal form of early, progressive dementia, Nasu-Hakola disease, and with an increased risk of Alzheimer's disease. Microglial defects in phagocytosis of toxic aggregates or apoptotic membranes were proposed to be at the origin of the pathological processes in the presence of Trem2 inactivating mutations. Here, we show that TREM2 is essential for microglia-mediated synaptic refinement during the early stages of brain development. The absence of Trem2 resulted in impaired synapse elimination, accompanied by enhanced excitatory neurotransmission and reduced long-range functional connectivity. Trem2-/- mice displayed repetitive behavior and altered sociability. TREM2 protein levels were also negatively correlated with the severity of symptoms in humans affected by autism. These data unveil the role of TREM2 in neuronal circuit sculpting and provide the evidence for the receptor's involvement in neurodevelopmental diseases.

Funding information:
  • NCI NIH HHS - CA156700(United States)

Dicer Deficiency Differentially Impacts Microglia of the Developing and Adult Brain.

  • Varol D
  • Immunity
  • 2017 Jun 20

Literature context:


Abstract:

Microglia seed the embryonic neuro-epithelium, expand and actively sculpt neuronal circuits in the developing central nervous system, but eventually adopt relative quiescence and ramified morphology in the adult. Here, we probed the impact of post-transcriptional control by microRNAs (miRNAs) on microglial performance during development and adulthood by generating mice lacking microglial Dicer expression at these distinct stages. Conditional Dicer ablation in adult microglia revealed that miRNAs were required to limit microglial responses to challenge. After peripheral endotoxin exposure, Dicer-deficient microglia expressed more pro-inflammatory cytokines than wild-type microglia and thereby compromised hippocampal neuronal functions. In contrast, prenatal Dicer ablation resulted in spontaneous microglia activation and revealed a role for Dicer in DNA repair and preservation of genome integrity. Accordingly, Dicer deficiency rendered otherwise radio-resistant microglia sensitive to gamma irradiation. Collectively, the differential impact of the Dicer ablation on microglia of the developing and adult brain highlights the changes these cells undergo with time.

Funding information:
  • NINDS NIH HHS - R37 NS041280(United States)

Macrophages Facilitate Electrical Conduction in the Heart.

  • Hulsmans M
  • Cell
  • 2017 Apr 20

Literature context:


Abstract:

Organ-specific functions of tissue-resident macrophages in the steady-state heart are unknown. Here, we show that cardiac macrophages facilitate electrical conduction through the distal atrioventricular node, where conducting cells densely intersperse with elongated macrophages expressing connexin 43. When coupled to spontaneously beating cardiomyocytes via connexin-43-containing gap junctions, cardiac macrophages have a negative resting membrane potential and depolarize in synchrony with cardiomyocytes. Conversely, macrophages render the resting membrane potential of cardiomyocytes more positive and, according to computational modeling, accelerate their repolarization. Photostimulation of channelrhodopsin-2-expressing macrophages improves atrioventricular conduction, whereas conditional deletion of connexin 43 in macrophages and congenital lack of macrophages delay atrioventricular conduction. In the Cd11bDTR mouse, macrophage ablation induces progressive atrioventricular block. These observations implicate macrophages in normal and aberrant cardiac conduction.

Funding information:
  • NHLBI NIH HHS - K24 HL105780()
  • NHLBI NIH HHS - R01 HL092577()
  • NHLBI NIH HHS - R01 HL096576()
  • NHLBI NIH HHS - R01 HL114477()
  • NHLBI NIH HHS - R01 HL117829()
  • NHLBI NIH HHS - R01 HL125428()
  • NHLBI NIH HHS - R01 HL128264()
  • NHLBI NIH HHS - R01 HL131495()
  • NICHD NIH HHS - R01 HD069623()
  • NIDDK NIH HHS - P30 DK043351()
  • NIDDK NIH HHS - P30 DK057521()
  • NINDS NIH HHS - R01 NS084863()

Huntingtin is required for normal excitatory synapse development in cortical and striatal circuits.

  • McKinstry SU
  • J. Neurosci.
  • 2014 Jul 9

Literature context:


Abstract:

Huntington's disease (HD) is a neurodegenerative disease caused by the expansion of a poly-glutamine (poly-Q) stretch in the huntingtin (Htt) protein. Gain-of-function effects of mutant Htt have been extensively investigated as the major driver of neurodegeneration in HD. However, loss-of-function effects of poly-Q mutations recently emerged as potential drivers of disease pathophysiology. Early synaptic problems in the excitatory cortical and striatal connections have been reported in HD, but the role of Htt protein in synaptic connectivity was unknown. Therefore, we investigated the role of Htt in synaptic connectivity in vivo by conditionally silencing Htt in the developing mouse cortex. When cortical Htt function was silenced, cortical and striatal excitatory synapses formed and matured at an accelerated pace through postnatal day 21 (P21). This exuberant synaptic connectivity was lost over time in the cortex, resulting in the deterioration of synapses by 5 weeks. Synaptic decline in the cortex was accompanied with layer- and region-specific reactive gliosis without cell loss. To determine whether the disease-causing poly-Q mutation in Htt affects synapse development, we next investigated the synaptic connectivity in a full-length knock-in mouse model of HD, the zQ175 mouse. Similar to the cortical conditional knock-outs, we found excessive excitatory synapse formation and maturation in the cortices of P21 zQ175, which was lost by 5 weeks. Together, our findings reveal that cortical Htt is required for the correct establishment of cortical and striatal excitatory circuits, and this function of Htt is lost when the mutant Htt is present.

Funding information:
  • NIGMS NIH HHS - R01 GM072881(United States)