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CC10 (T-18) antibody

RRID:AB_2238819

Antibody ID

AB_2238819

Target Antigen

CC10 (T-18) human, mouse, rat, mouse, rat, human

Proper Citation

(Santa Cruz Biotechnology Cat# sc-9772, RRID:AB_2238819)

Clonality

polyclonal antibody

Comments

Discontinued: 2016; validation status unknown check with seller; recommendations: ELISA; Immunofluorescence; Western Blot; WB, IP, IF, ELISA

Host Organism

goat

Vendor

Santa Cruz Biotechnology

Cat Num

sc-9772

Publications that use this research resource

Myoepithelial Cells of Submucosal Glands Can Function as Reserve Stem Cells to Regenerate Airways after Injury.

  • Tata A
  • Cell Stem Cell
  • 2018 May 3

Literature context:


Abstract:

Cells demonstrate plasticity following injury, but the extent of this phenomenon and the cellular mechanisms involved remain underexplored. Using single-cell RNA sequencing (scRNA-seq) and lineage tracing, we uncover that myoepithelial cells (MECs) of the submucosal glands (SMGs) proliferate and migrate to repopulate the airway surface epithelium (SE) in multiple injury models. Specifically, SMG-derived cells display multipotency and contribute to basal and luminal cell types of the SMGs and SE. Ex vivo expanded MECs have the potential to repopulate and differentiate into SE cells when grafted onto denuded airway scaffolds. Significantly, we find that SMG-like cells appear on the SE of both extra- and intra-lobular airways of large animal lungs following severe injury. We find that the transcription factor SOX9 is necessary for MEC plasticity in airway regeneration. Because SMGs are abundant and present deep within airways, they may serve as a reserve cell source for enhancing human airway regeneration.

Funding information:
  • NHLBI NIH HHS - R00 HL127181()
  • NIDDK NIH HHS - DK59630(United States)
  • NIEHS NIH HHS - U01 ES017219()

Spatial-Temporal Lineage Restrictions of Embryonic p63+ Progenitors Establish Distinct Stem Cell Pools in Adult Airways.

  • Yang Y
  • Dev. Cell
  • 2018 Mar 26

Literature context:


Abstract:

Basal cells (BCs) are p63-expressing multipotent progenitors of skin, tracheoesophageal and urinary tracts. p63 is abundant in developing airways; however, it remains largely unclear how embryonic p63+ cells contribute to the developing and postnatal respiratory tract epithelium, and ultimately how they relate to adult BCs. Using lineage-tracing and functional approaches in vivo, we show that p63+ cells arising from the lung primordium are initially multipotent progenitors of airway and alveolar lineages but later become restricted proximally to generate the tracheal adult stem cell pool. In intrapulmonary airways, these cells are maintained immature to adulthood in bronchi, establishing a rare p63+Krt5- progenitor cell population that responds to H1N1 virus-induced severe injury. Intriguingly, this pool includes a CC10 lineage-labeled p63+Krt5- cell subpopulation required for a full H1N1-response. These data elucidate key aspects in the establishment of regionally distinct adult stem cell pools in the respiratory system, potentially with relevance to other organs.

Funding information:
  • Intramural NIH HHS - ZIA HL006151-02(United States)
  • NCI NIH HHS - R01 CA112403()
  • NCI NIH HHS - R01 CA193455()
  • NHLBI NIH HHS - R35 HL135834()
  • NIAID NIH HHS - HHSN272201400008C()

Developmental History Provides a Roadmap for the Emergence of Tumor Plasticity.

  • Tata PR
  • Dev. Cell
  • 2018 Mar 26

Literature context:


Abstract:

We show that the loss or gain of transcription factor programs that govern embryonic cell-fate specification is associated with a form of tumor plasticity characterized by the acquisition of alternative cell fates normally characteristic of adjacent organs. In human non-small cell lung cancers, downregulation of the lung lineage-specifying TF NKX2-1 is associated with tumors bearing features of various gut tissues. Loss of Nkx2-1 from murine alveolar, but not airway, epithelium results in conversion of lung cells to gastric-like cells. Superimposing oncogenic Kras activation enables further plasticity in both alveolar and airway epithelium, producing tumors that adopt midgut and hindgut fates. Conversely, coupling Nkx2-1 loss with foregut lineage-specifying SOX2 overexpression drives the formation of squamous cancers with features of esophageal differentiation. These findings demonstrate that elements of pathologic tumor plasticity mirror the normal developmental history of organs in that cancer cells acquire cell fates associated with developmentally related neighboring organs.

Funding information:
  • NCI NIH HHS - R01CA172025(United States)
  • NHLBI NIH HHS - K99 HL127181()
  • NHLBI NIH HHS - P30 HL101287()
  • NHLBI NIH HHS - R00 HL127181()
  • NHLBI NIH HHS - R01 HL118185()
  • NIGMS NIH HHS - T32 GM007205()

mTORC1 Activation during Repeated Regeneration Impairs Somatic Stem Cell Maintenance.

  • Haller S
  • Cell Stem Cell
  • 2017 Dec 7

Literature context:


Abstract:

The balance between self-renewal and differentiation ensures long-term maintenance of stem cell (SC) pools in regenerating epithelial tissues. This balance is challenged during periods of high regenerative pressure and is often compromised in aged animals. Here, we show that target of rapamycin (TOR) signaling is a key regulator of SC loss during repeated regenerative episodes. In response to regenerative stimuli, SCs in the intestinal epithelium of the fly and in the tracheal epithelium of mice exhibit transient activation of TOR signaling. Although this activation is required for SCs to rapidly proliferate in response to damage, repeated rounds of damage lead to SC loss. Consistently, age-related SC loss in the mouse trachea and in muscle can be prevented by pharmacologic or genetic inhibition, respectively, of mammalian target of rapamycin complex 1 (mTORC1) signaling. These findings highlight an evolutionarily conserved role of TOR signaling in SC function and identify repeated rounds of mTORC1 activation as a driver of age-related SC decline.

Funding information:
  • BLRD VA - I01 BX002324()
  • NCRR NIH HHS - UL1 RR024989(United States)
  • NHLBI NIH HHS - R01 HL132996()
  • NIA NIH HHS - K99 AG041764()
  • NIA NIH HHS - P01 AG036695()
  • NIA NIH HHS - R00 AG041764()
  • NIA NIH HHS - R01 AG047497()
  • NIA NIH HHS - R01 AG047820()
  • NIA NIH HHS - R37 AG023806()
  • NIDDK NIH HHS - R01 DK100342()
  • NIDDK NIH HHS - R01 DK113144()

Fgf10-Hippo Epithelial-Mesenchymal Crosstalk Maintains and Recruits Lung Basal Stem Cells.

  • Volckaert T
  • Dev. Cell
  • 2017 Oct 9

Literature context:


Abstract:

The lung harbors its basal stem/progenitor cells (BSCs) in the protected environment of the cartilaginous airways. After major lung injuries, BSCs are activated and recruited to sites of injury. Here, we show that during homeostasis, BSCs in cartilaginous airways maintain their stem cell state by downregulating the Hippo pathway (resulting in increased nuclear Yap), which generates a localized Fgf10-expressing stromal niche; in contrast, differentiated epithelial cells in non-cartilaginous airways maintain quiescence by activating the Hippo pathway and inhibiting Fgf10 expression in airway smooth muscle cells (ASMCs). However, upon injury, surviving differentiated epithelial cells spread to maintain barrier function and recruit integrin-linked kinase to adhesion sites, which leads to Merlin degradation, downregulation of the Hippo pathway, nuclear Yap translocation, and expression and secretion of Wnt7b. Epithelial-derived Wnt7b, then in turn, induces Fgf10 expression in ASMCs, which extends the BSC niche to promote regeneration.

Funding information:
  • NHLBI NIH HHS - R01 HL092967()
  • NHLBI NIH HHS - R01 HL126732()
  • NHLBI NIH HHS - R01 HL132156()

Anatomically and Functionally Distinct Lung Mesenchymal Populations Marked by Lgr5 and Lgr6.

  • Lee JH
  • Cell
  • 2017 Sep 7

Literature context:


Abstract:

The diversity of mesenchymal cell types in the lung that influence epithelial homeostasis and regeneration is poorly defined. We used genetic lineage tracing, single-cell RNA sequencing, and organoid culture approaches to show that Lgr5 and Lgr6, well-known markers of stem cells in epithelial tissues, are markers of mesenchymal cells in the adult lung. Lgr6+ cells comprise a subpopulation of smooth muscle cells surrounding airway epithelia and promote airway differentiation of epithelial progenitors via Wnt-Fgf10 cooperation. Genetic ablation of Lgr6+ cells impairs airway injury repair in vivo. Distinct Lgr5+ cells are located in alveolar compartments and are sufficient to promote alveolar differentiation of epithelial progenitors through Wnt activation. Modulating Wnt activity altered differentiation outcomes specified by mesenchymal cells. This identification of region- and lineage-specific crosstalk between epithelium and their neighboring mesenchymal partners provides new understanding of how different cell types are maintained in the adult lung.

Funding information:
  • NCI NIH HHS - K99 CA187317()
  • NCI NIH HHS - P30 CA014051()
  • NCI NIH HHS - U24 CA180922()
  • NHLBI NIH HHS - R01 HL090136()
  • NHLBI NIH HHS - R01 HL125821()
  • NHLBI NIH HHS - U01 HL100402()
  • Wellcome Trust - R01 HL132266()