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Goat anti-Rat IgG (H+L) Cross-Adsorbed Secondary Antibody, Alexa Fluor 633


Antibody ID


Target Antigen

Rat IgG (H+L) Cross-Adsorbed rat

Proper Citation

(Thermo Fisher Scientific Cat# A-21094, RRID:AB_2535749)


polyclonal antibody


Applications: ICC (2 µg/mL), IHC (1-10 µg/mL), IF (2 µg/mL)

Host Organism



Thermo Fisher Scientific Go To Vendor

Drosophila TNF Modulates Tissue Tension in the Embryo to Facilitate Macrophage Invasive Migration.

  • Ratheesh A
  • Dev. Cell
  • 2018 May 7

Literature context: Fisher Scientific Cat# A-21094, RRID:AB_2535749 Alexa Fluor 488 goat anti-rat T


Migrating cells penetrate tissue barriers during development, inflammatory responses, and tumor metastasis. We study if migration in vivo in such three-dimensionally confined environments requires changes in the mechanical properties of the surrounding cells using embryonic Drosophila melanogaster hemocytes, also called macrophages, as a model. We find that macrophage invasion into the germband through transient separation of the apposing ectoderm and mesoderm requires cell deformations and reductions in apical tension in the ectoderm. Interestingly, the genetic pathway governing these mechanical shifts acts downstream of the only known tumor necrosis factor superfamily member in Drosophila, Eiger, and its receptor, Grindelwald. Eiger-Grindelwald signaling reduces levels of active Myosin in the germband ectodermal cortex through the localization of a Crumbs complex component, Patj (Pals-1-associated tight junction protein). We therefore elucidate a distinct molecular pathway that controls tissue tension and demonstrate the importance of such regulation for invasive migration in vivo.

Funding information:
  • NCI NIH HHS - P50 CA130805(United States)

Activating the regenerative potential of Müller glia cells in a regeneration-deficient retina.

  • Lust K
  • Elife
  • 2018 Jan 29

Literature context: 633 (goat)Thermo FisherA-21094, RRID: AB_25357491: 750Recombinant DNA reagentrx2


Regeneration responses in animals are widespread across phyla. To identify molecular players that confer regenerative capacities to non-regenerative species is of key relevance for basic research and translational approaches. Here, we report a differential response in retinal regeneration between medaka (Oryzias latipes) and zebrafish (Danio rerio). In contrast to zebrafish, medaka Müller glia (olMG) cells behave like progenitors and exhibit a restricted capacity to regenerate the retina. After injury, olMG cells proliferate but fail to self-renew and ultimately only restore photoreceptors. In our injury paradigm, we observed that in contrast to zebrafish, proliferating olMG cells do not maintain sox2 expression. Sustained sox2 expression in olMG cells confers regenerative responses similar to those of zebrafish MG (drMG) cells. We show that a single, cell-autonomous factor reprograms olMG cells and establishes a regeneration-like mode. Our results position medaka as an attractive model to delineate key regeneration factors with translational potential.

Funding information:
  • NIMH NIH HHS - R01 MH073991(United States)

Feature Integration Drives Probabilistic Behavior in the Drosophila Escape Response.

  • von Reyn CR
  • Neuron
  • 2017 Jun 21

Literature context: A-21094; RRID:AB_2535749 Alexa 633


Animals rely on dedicated sensory circuits to extract and encode environmental features. How individual neurons integrate and translate these features into behavioral responses remains a major question. Here, we identify a visual projection neuron type that conveys predator approach information to the Drosophila giant fiber (GF) escape circuit. Genetic removal of this input during looming stimuli reveals that it encodes angular expansion velocity, whereas other input cell type(s) encode angular size. Motor program selection and timing emerge from linear integration of these two features within the GF. Linear integration improves size detection invariance over prior models and appropriately biases motor selection to rapid, GF-mediated escapes during fast looms. Our findings suggest feature integration, and motor control may occur as simultaneous operations within the same neuron and establish the Drosophila escape circuit as a model system in which these computations may be further dissected at the circuit level. VIDEO ABSTRACT.

Amitosis of Polyploid Cells Regenerates Functional Stem Cells in the Drosophila Intestine.

  • Lucchetta EM
  • Cell Stem Cell
  • 2017 May 4

Literature context: # A21094; RRID:AB_2535749 Chemicals,


Organ fitness depends on appropriate maintenance of stem cell populations, and aberrations in functional stem cell numbers are associated with malignancies and aging. Symmetrical division is the best characterized mechanism of stem cell replacement, but other mechanisms could also be deployed, particularly in situations of high stress. Here, we show that after severe depletion, intestinal stem cells (ISCs) in the Drosophila midgut are replaced by spindle-independent ploidy reduction of cells in the enterocyte lineage through a process known as amitosis. Amitosis is also induced by the functional loss of ISCs coupled with tissue demand and in aging flies, underscoring the generality of this mechanism. However, we also found that random homologous chromosome segregation during ploidy reduction can expose deleterious mutations through loss of heterozygosity. Together, our results highlight amitosis as an unappreciated mechanism for restoring stem cell homeostasis, but one with some associated risk in animals carrying mutations.

Funding information:
  • NICHD NIH HHS - T32 HD055165()
  • NIDDK NIH HHS - R01 DK107702()

Phosphatidylserine Exposure Controls Viral Innate Immune Responses by Microglia.

  • Tufail Y
  • Neuron
  • 2017 Feb 8

Literature context: #A-21094; RRID:AB_2535749), and Alex


Microglia are the intrinsic immune sentinels of the central nervous system. Their activation restricts tissue injury and pathogen spread, but in some settings, including viral infection, this response can contribute to cell death and disease. Identifying mechanisms that control microglial responses is therefore an important objective. Using replication-incompetent adenovirus 5 (Ad5)-based vectors as a model, we investigated the mechanisms through which microglia recognize and respond to viral uptake. Transgenic, immunohistochemical, molecular-genetic, and fluorescence imaging approaches revealed that phosphatidylserine (PtdSer) exposure on the outer leaflet of transduced cells triggers their engulfment by microglia through TAM receptor-dependent mechanisms. We show that inhibition of phospholipid scramblase 1 (PLSCR1) activity reduces intracellular calcium dysregulation, prevents PtdSer externalization, and enables months-long protection of vector-transduced, transgene-expressing cells from microglial phagocytosis. Our study identifies PLSCR1 as a potent target through which the innate immune response to viral vectors, and potentially other stimuli, may be controlled.

Funding information:
  • NIAID NIH HHS - R01 AI101400()
  • NINDS NIH HHS - DP2 NS083038()
  • NINDS NIH HHS - R01 NS085296()
  • NINDS NIH HHS - R01 NS085938()