X
Forgot Password

If you have forgotten your password you can enter your email here and get a temporary password sent to your email.

Alexa Fluor 594-Streptavidin antibody

RRID:AB_2337250

Antibody ID

AB_2337250

Target Antigen

Streptavidin

Proper Citation

(Jackson ImmunoResearch Labs Cat# 016-580-084, RRID:AB_2337250)

Clonality

unknown

Comments

Originating manufacturer of this product

Vendor

Jackson ImmunoResearch Labs Go To Vendor

Cat Num

016-580-084

Publications that use this research resource

Reducing Pericyte-Derived Scarring Promotes Recovery after Spinal Cord Injury.

  • Dias DO
  • Cell
  • 2018 Mar 22

Literature context:


Abstract:

CNS injury often severs axons. Scar tissue that forms locally at the lesion site is thought to block axonal regeneration, resulting in permanent functional deficits. We report that inhibiting the generation of progeny by a subclass of pericytes led to decreased fibrosis and extracellular matrix deposition after spinal cord injury in mice. Regeneration of raphespinal and corticospinal tract axons was enhanced and sensorimotor function recovery improved following spinal cord injury in animals with attenuated pericyte-derived scarring. Using optogenetic stimulation, we demonstrate that regenerated corticospinal tract axons integrated into the local spinal cord circuitry below the lesion site. The number of regenerated axons correlated with improved sensorimotor function recovery. In conclusion, attenuation of pericyte-derived fibrosis represents a promising therapeutic approach to facilitate recovery following CNS injury.

Funding information:
  • Intramural NIH HHS - Z01 DE000698-10(United States)

Redirection of neuroblast migration from the rostral migratory stream into a lesion in the prefrontal cortex of adult rats.

  • Gundelach J
  • Exp Brain Res
  • 2018 Feb 23

Literature context:


Abstract:

Clinical treatment of structural brain damage today is largely limited to symptomatic approaches and the avoidance of secondary injury. However, neuronal precursor cells are constantly produced within specified regions of the mammalian brain throughout life. Here we evaluate the potential of the known chemoattractive properties of the glycoprotein laminin on neuroblasts to relocate the cells into damaged brain areas. Injection of a thin laminin tract, leading from the rostral migratory stream to an excitotoxic lesion within the medial prefrontal cortex of rats, enabled neuroblasts to migrate away from their physiological route towards the olfactory bulb into the lesion site. Once they reached the damaged tissue, they migrated further in a non-uniform orientation within the lesion. Furthermore, our data indicate that the process of diverted migration is still active 6 weeks after the treatment and that at least some of the neuroblasts are capable of maturing into adult neurons.

Funding information:
  • NIAID NIH HHS - AI053108(United States)

Human embryonic lung epithelial tips are multipotent progenitors that can be expanded in vitro as long-term self-renewing organoids.

  • Nikolić MZ
  • Elife
  • 2017 Jun 30

Literature context:


Abstract:

The embryonic mouse lung is a widely used substitute for human lung development. For example, attempts to differentiate human pluripotent stem cells to lung epithelium rely on passing through progenitor states that have only been described in mouse. The tip epithelium of the branching mouse lung is a multipotent progenitor pool that self-renews and produces differentiating descendants. We hypothesized that the human distal tip epithelium is an analogous progenitor population and tested this by examining morphology, gene expression and in vitro self-renewal and differentiation capacity of human tips. These experiments confirm that human and mouse tips are analogous and identify signalling pathways that are sufficient for long-term self-renewal of human tips as differentiation-competent organoids. Moreover, we identify mouse-human differences, including markers that define progenitor states and signalling requirements for long-term self-renewal. Our organoid system provides a genetically-tractable tool that will allow these human-specific features of lung development to be investigated.

Agonist-evoked Ca2+ signaling in enteric glia drives neural programs that regulate intestinal motility in mice.

  • McClain JL
  • Cell Mol Gastroenterol Hepatol
  • 2015 Nov 1

Literature context:


Abstract:

BACKGROUND & AIMS: Gastrointestinal motility is regulated by enteric neural circuitry that includes enteric neurons and glia. Enteric glia monitor synaptic activity and exhibit responses to neurotransmitters that are encoded by intracellular calcium (Ca2+) signaling. What role evoked glial responses play in the neural regulation of gut motility is unknown. We tested how evoking Ca2+ signaling in enteric glia affects the neural control of intestinal motility. METHODS: We used a novel chemogenetic mouse model that expresses the designer receptor hM3Dq under the transcriptional control of the glial fibrillary acidic protein (GFAP) promoter (GFAP::hM3Dq mice) to selectively trigger glial Ca2+ signaling. We used in situ Ca2+ imaging and immunohistochemistry to validate this model and assessed gut motility by measuring pellet output and composition, colonic bead expulsion time, small intestinal transit time, total gut transit time, colonic migrating motor complex (CMMC) recordings and muscle tension recordings. RESULTS: hM3Dq receptor expression is confined to GFAP-positive enteric glia in the intestines of GFAP::hM3Dq mice. In these mice, application of the hM3Dq agonist clozapine-N-oxide (CNO) selectively triggers intracellular Ca2+ responses in enteric glia. Glial activation drove neurogenic contractions in the ileum and colon but had no effect on neurogenic relaxations. CNO enhanced the amplitude and frequency of CMMCs in ex vivo preparations of the colon and CNO increased colonic motility in vivo. CNO had no effect on the composition of fecal matter, small intestinal transit or whole gut transit. CONCLUSIONS: Glial excitability encoded by intracellular Ca2+ signaling functions to modulate excitatory enteric circuits. Selectively triggering glial Ca2+ signaling might be a novel strategy to improve gut function in motility disorders.