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pp120 antibody

RRID:AB_397537

Antibody ID

AB_397537

Target Antigen

pp120 mouse, chicken/bird, canine, human, rat, chicken, dog, human, mouse, rat

Proper Citation

(BD Biosciences Cat# 610134, RRID:AB_397537)

Clonality

monoclonal antibody

Comments

Immunofluorescence, Western blot

Host Organism

mouse

Vendor

BD Biosciences Go To Vendor

Cat Num

610134

Publications that use this research resource

Localization of nectin-2α at the boundary between the adjacent somata of the clustered cholinergic neurons and its regulatory role in the subcellular localization of the voltage-gated A-type K+ channel Kv4.2 in the medial habenula.

  • Shiotani H
  • J. Comp. Neurol.
  • 2018 Jun 15

Literature context:


Abstract:

The medial habenula (MHb), implicated in stress, depression, memory, and nicotine withdrawal syndromes, receives septal inputs and sends efferents to the interpeduncular nucleus. We previously showed that the immunoglobulin-like cell adhesion molecules (CAMs) nectin-2α and nectin-2δ are expressed in astrocytes in the brain, but their expression in neurons remains unknown. We showed here by immunofluorescence microscopy that nectin-2α, but not nectin-2δ, was prominently expressed in the cholinergic neurons in the developing and adult MHbs and localized at the boundary between the adjacent somata of the clustered cholinergic neurons where the voltage-gated A-type K+ channel Kv4.2 was localized. Analysis by immunoelectron microscopy on this boundary revealed that Kv4.2 was localized at the membrane specializations (MSs) with plasma membrane darkening in an asymmetrical manner, whereas nectin-2α was localized on the apposed plasma membranes mostly at the outside of these MSs, but occasionally localized at their edges and insides. Nectin-2α at this boundary was not colocalized with the nectin-2α-binding protein afadin, other CAMs, or their interacting peripheral membrane proteins, suggesting that nectin-2α forms a cell adhesion apparatus different from the Kv4.2-associated MSs. Genetic ablation of nectin-2 delayed the localization of Kv4.2 at the boundary between the adjacent somata of the clustered cholinergic neurons in the developing MHb. These results revealed the unique localization of nectin-2α and its regulatory role in the localization of Kv4.2 at the MSs in the MHb.

Funding information:
  • Howard Hughes Medical Institute - (United States)

Regulation of Epithelial Plasticity Determines Metastatic Organotropism in Pancreatic Cancer.

  • Reichert M
  • Dev. Cell
  • 2018 Jun 18

Literature context:


Abstract:

The regulation of metastatic organotropism in pancreatic ductal a denocarcinoma (PDAC) remains poorly understood. We demonstrate, using multiple mouse models, that liver and lung metastatic organotropism is dependent upon p120catenin (p120ctn)-mediated epithelial identity. Mono-allelic p120ctn loss accelerates KrasG12D-driven pancreatic cancer formation and liver metastasis. Importantly, one p120ctn allele is sufficient for E-CADHERIN-mediated cell adhesion. By contrast, cells with bi-allelic p120ctn loss demonstrate marked lung organotropism; however, rescue with p120ctn isoform 1A restores liver metastasis. In a p120ctn-independent PDAC model, mosaic loss of E-CADHERIN expression reveals selective pressure for E-CADHERIN-positive liver metastasis and E-CADHERIN-negative lung metastasis. Furthermore, human PDAC and liver metastases support the premise that liver metastases exhibit predominantly epithelial characteristics. RNA-seq demonstrates differential induction of pathways associated with metastasis and epithelial-to-mesenchymal transition in p120ctn-deficient versus p120ctn-wild-type cells. Taken together, P120CTN and E-CADHERIN mediated epithelial plasticity is an addition to the conceptual framework underlying metastatic organotropism in pancreatic cancer.

Funding information:
  • NCI NIH HHS - F30 CA180601()
  • NCI NIH HHS - F32 CA221094()
  • NIDDK NIH HHS - P30 DK050306()
  • NIDDK NIH HHS - R01 DK060694()
  • NIDDK NIH HHS - R21DK090778(United States)

Detachment of Chain-Forming Neuroblasts by Fyn-Mediated Control of cell-cell Adhesion in the Postnatal Brain.

  • Fujikake K
  • J. Neurosci.
  • 2018 May 9

Literature context:


Abstract:

In the rodent olfactory system, neuroblasts produced in the ventricular-subventricular zone of the postnatal brain migrate tangentially in chain-like cell aggregates toward the olfactory bulb (OB) through the rostral migratory stream (RMS). After reaching the OB, the chains are dissociated and the neuroblasts migrate individually and radially toward their final destination. The cellular and molecular mechanisms controlling cell-cell adhesion during this detachment remain unclear. Here we report that Fyn, a nonreceptor tyrosine kinase, regulates the detachment of neuroblasts from chains in the male and female mouse OB. By performing chemical screening and in vivo loss-of-function and gain-of-function experiments, we found that Fyn promotes somal disengagement from the chains and is involved in neuronal migration from the RMS into the granule cell layer of the OB. Fyn knockdown or Dab1 (disabled-1) deficiency caused p120-catenin to accumulate and adherens junction-like structures to be sustained at the contact sites between neuroblasts. Moreover, a Fyn and N-cadherin double-knockdown experiment indicated that Fyn regulates the N-cadherin-mediated cell adhesion between neuroblasts. These results suggest that the Fyn-mediated control of cell-cell adhesion is critical for the detachment of chain-forming neuroblasts in the postnatal OB.SIGNIFICANCE STATEMENT In the postnatal brain, newly born neurons (neuroblasts) migrate in chain-like cell aggregates toward their destination, where they are dissociated into individual cells and mature. The cellular and molecular mechanisms controlling the detachment of neuroblasts from chains are not understood. Here we show that Fyn, a nonreceptor tyrosine kinase, promotes the somal detachment of neuroblasts from chains, and that this regulation is critical for the efficient migration of neuroblasts to their destination. We further show that Fyn and Dab1 (disabled-1) decrease the cell-cell adhesion between chain-forming neuroblasts, which involves adherens junction-like structures. Our results suggest that Fyn-mediated regulation of the cell-cell adhesion of neuroblasts is critical for their detachment from chains in the postnatal brain.

Funding information:
  • NCCIH NIH HHS - 5R01AT006732(United States)

Insm1 Induces Neural Progenitor Delamination in Developing Neocortex via Downregulation of the Adherens Junction Belt-Specific Protein Plekha7.

  • Tavano S
  • Neuron
  • 2018 Mar 21

Literature context:


Abstract:

Delamination of neural progenitor cells (NPCs) from the ventricular surface is a crucial prerequisite to form the subventricular zone, the germinal layer linked to the expansion of the mammalian neocortex in development and evolution. Here, we dissect the molecular mechanism by which the transcription factor Insm1 promotes the generation of basal progenitors (BPs). Insm1 protein is most highly expressed in newborn BPs in mouse and human developing neocortex. Forced Insm1 expression in embryonic mouse neocortex causes NPC delamination, converting apical to basal radial glia. Insm1 represses the expression of the apical adherens junction belt-specific protein Plekha7. CRISPR/Cas9-mediated disruption of Plekha7 expression suffices to cause NPC delamination. Plekha7 overexpression impedes the intrinsic and counteracts the Insm1-induced, NPC delamination. Our findings uncover a novel molecular mechanism underlying NPC delamination in which a BP-genic transcription factor specifically targets the integrity of the apical adherens junction belt, rather than adherens junction components as such.

Funding information:
  • Intramural NIH HHS - ZIA BC010763-05(United States)

Canonical Wnt/β-Catenin Signaling Regulates Postnatal Mouse Epididymal Development But Does Not Affect Epithelial Cell Differentiation.

  • Kumar M
  • Endocrinology
  • 2017 Dec 1

Literature context:


Abstract:

The epithelial lining of the epididymis establishes an optimal environment in which spermatozoa acquire the ability to fertilize an oocyte. This highly specialized organ develops from a simple embryonic tube known as the Wolffian duct (WD). How the simple columnar epithelium of WD acquires the complex features of the adult epididymal epithelium is currently unclear. During these first few weeks after birth, the epididymal epithelium undergoes major changes and by 5 weeks consists of four different cell types. The main objective of this study was to evaluate potential roles of Wnt signaling during postnatal epididymal development and differentiation. To analyze the activity of Wnt signaling during postnatal development, we evaluated the epididymis of TCFGFP mice, a Wnt reporter mouse model. Wnt signaling activity as indicated by green fluorescent protein expression was detected in the whole epididymis of TCFGFP mice during the first 2 weeks of life but was localized only to the caput region by 5 weeks of age. Using a genetic cell lineage tracing approach, we showed that all four of the epididymal epithelial cell types originated from the simple columnar epithelium of WD. To delineate the functional significance of epithelial Wnt signaling in epididymal development and differentiation, we generated a mouse model in which β-catenin (Ctnnb1) was specifically ablated from the epididymal epithelium upon administration of doxycycline. Genetic suppression of epithelial Wnt/β-catenin signaling inhibited epididymal development by affecting cell proliferation but had no effect on epithelial cell differentiation.

Funding information:
  • NINDS NIH HHS - NS041218(United States)

Axon behavior in the olfactory nerve reflects the involvement of catenin-cadherin mediated adhesion.

  • Akins MR
  • J. Comp. Neurol.
  • 2006 Dec 20

Literature context:


Abstract:

The projection of olfactory sensory neuron (OSN) axons to the olfactory bulb (OB) is a complex but well-regulated process. Although odorant receptor proteins, and other molecules, are implicated in this process, our understanding remains incomplete. We demonstrate that axons remain restricted to the outer olfactory nerve layer (ONLo) until they are proximal to their target glomeruli, where they enter the inner ONL (ONLi), dividing the ONL into extension and sorting zones. Sorting is likely contingent on cell:cell interactions mediated in part by cell adhesion molecules. The cadherins are a large family of adhesion molecules whose function is contingent on their intracellular binding partners, the catenins, which in turn link to the cytoskeleton. We previously demonstrated that the organization of the cytoskeleton changed as olfactory sensory neuron axons moved from the ONLo to the ONLi. To further assess the role of cadherin mediated adhesion in the developing mouse ONL, we localized alpha-, beta-, gamma-, delta-, and p120-catenins as well as neural cadherin (N-cadherin; CDH2) in the OB. alpha- and beta-catenins are found throughout the OB and are uniform throughout the ONL. In contrast, gamma-catenin and CDH2 are expressed predominantly in the ONLo during perinatal development, but are uniform across the ONL beginning at P7 and into adulthood. Finally, p120- and delta-catenins are expressed in nonoverlapping patterns by olfactory axons and OB neuronal dendrites, respectively. We conclude that gamma-catenin-mediated CDH2 adhesion may influence OSN targeting by restricting axons to the ONLo until they reach the appropriate domain of the OB.

Funding information:
  • NIEHS NIH HHS - Z01 ES065073(United States)