The Protein Kinase C Family: Key Regulators Bridging Signaling Pathways in Skin and Tumor Epithelia

Breitkreutz, Dirk; Braiman-Wiksman, Liora; Daum, Nicole; Tennenbaum, Tamar

doi:10.1007/978-1-4419-6382-6_8

Cited by 1 publication

(1 citation statement)

References 243 publications

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“…As a result that PKC-ε has an actin-binding motif at amino acids 223-228, we sought to determine whether actin binding was influencing enzyme location by comparing PKC to a protein whose actin-binding characteristics are well understood. We chose vinculin for this purpose because both the actin-binding domain and a phosphorylation site for PKC are exposed when the vinculin molecule unfolds [35]. The actin-binding domain of vinculin is critical to its functions, for example, slowing retrograde flow of the actin subunits [36].…”

Section: Pkc Locations Are Dictated In Part By Actin Bindingmentioning

confidence: 99%

Activated Protein Kinase C (PKC) Is Persistently Trafficked with Epidermal Growth Factor (EGF) Receptor

et al. 2020

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Protein kinase Cs (PKCs) are activated by lipids in the plasma membrane and bind to a scaffold assembled on the epidermal growth factor (EGF) receptor (EGFR). Understanding how this complex is routed is important, because this determines whether EGFR is degraded, terminating signaling. Here, cells were preincubated in EGF-tagged gold nanoparticles, then allowed to internalize them in the presence or absence of a phorbol ester PKC activator. PKC colocalized with EGF-tagged nanoparticles within 5 min and migrated with EGFR-bearing vesicles into the cell. Two conformations of PKC-epsilon were distinguished by different primary antibodies. One, thought to be enzymatically active, was on endosomes and displayed a binding site for antibody RR (R&D). The other, recognized by Genetex green (GG), was soluble, on actin-rich structures, and loosely bound to vesicles. During a 15-min chase, EGF-tagged nanoparticles entered large, perinuclear structures. In phorbol ester-treated cells, vesicles bearing EGF-tagged nanoparticles tended to enter this endocytic recycling compartment (ERC) without the GG form. The correlation coefficient between the GG (inactive) and RR conformations on vesicles was also lower. Thus, active PKC has a Charon-like function, ferrying vesicles to the ERC, and inactivation counteracts this function. The advantage conferred on cells by aggregating vesicles in the ERC is unclear.

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Section: Pkc Locations Are Dictated In Part By Actin Bindingmentioning

confidence: 99%