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Cognition Enhancers
Published in Sahab Uddin, Rashid Mamunur, Advances in Neuropharmacology, 2020
Ramneek Kaur, Rashi Rajput, Sachin Kumar, Harleen Kaur, R. Rachana, Manisha Singh
The interaction between PKC isozymes and apoptosis pathways is quite convoluted. Though, PKCδ is considered as an apoptotic isozyme whereas, PKCδ restrains apoptosis which is induced by irradiation (Bluwstein et al., 2013) or oxidized low-density lipoprotein (LDL) (Larroque-Cardoso et al., 2013). Also, PKCε is an antagonist of PKCδ, the suppression of PKCε increases the cell death by obstructing the ability of PKC to inhibit BCL2 (B-cell lymphoma 2, an anti-apoptotic factor). Furthermore, caspases can cleave all types of PKC ε, δ, ζ, and θ (Basu and Sivaprasad, 2007; Mizuno et al., 1997; Datta et al., 1997; Smith et al., 2000). Therefore, further investigation is required to know how neuroprotective activity of PKC is dependent on apoptosis.
Postimplantation diabetic embryopathy
Published in Moshe Hod, Lois G. Jovanovic, Gian Carlo Di Renzo, Alberto de Leiva, Oded Langer, Textbook of Diabetes and Pregnancy, 2018
Ulf J. Eriksson, Parri Wentzel
It has been reported that PKC signaling is associated with apoptosis, especially the isoforms PKC-δ202 and PKC-ζ.203 It has further been suggested that PKC-δ is involved in stabilizing p53 proteins204 and that it is related to ROS production,205 both of which would ultimately lead to apoptotic cell death. Since enhanced apoptosis is a feature of diabetic embryopathy (see later), one study used addition of specific inhibitors of PKC-δ and PKC-ζ, to high-glucose culture medium and found diminished dysmorphogenesis.192 In a subsequent study with specific inhibitors of PKC-α, PKC-βII, and PKC-δ added to the high-glucose culture medium, it was shown that all of these inhibitors diminish embryonic dysmorphogenesis and decrease the glucose-enhanced activity of their respective PKC isoform.193 In a subsequent study, inhibition of PKC-βII in high glucose–cultured mouse embryos diminished the rate of NTD and also decreased several glucose-induced embryonic effects, such as activation of Bid, caspase 8 and 3, and cytochrome C release from mitochondria.194 Furthermore, in a recent study, female mice heterozygous for PKC-δ (pkcδ+/-) were made diabetic with streptozotocin (SZ) and mated with heterozygous males. The NTD rate in the diabetes-exposed homozygous (pkcδ-/-) embryos was markedly diminished compared with the rate of diabetes-exposed wild-type (pkcδ+/+) embryos.195 Also, the diabetes-exposed pkcδ−/− embryos had lower markers of oxidative stress, endoplasmic reticulum (ER) stress, as well as normalized expression of phosphorylated JNK (p-JNK).195
Cytokines, Apoptosis, and Immune Therapy in HIV Infection
Published in Thomas F. Kresina, Immune Modulating Agents, 2020
Jerôme Estaquier, Jean-Claude Ameisen
Ligation of Fas or binding of TNF to its receptor has recently been implicated as signaling intermediary proteins. Proteins such as Mort1/FADD, RIP, and TRADD bear death domains resembling those in CD95 and the p55 TNF receptor. The overexpression of these proteins induces apoptosis (see for review Refs. 117–119). The formation of complexed proteins through Fas or TNF activation induces the cell death machinery including the protease cascade. At the apex is FLICE/MACH1, recruited by FADD/MORT1, which primes for a second transcleavage. Activation of interleukin 1 converting enzyme (ICE) family-related proteases, the ICE subfamilly members formed by ICE, ICE rel III, and ICE rei II (also known as TX and ICH2), and the NEDD-2 family members ICH1, leads to a second protease cascade. One critical target of this cascade is CPP32β (also known as Yama, and Apopain). Other targets include subfamily members CPP32, Mch2, Mch3 (also known as ICE-LAP-3 and CMH-1), and Mch4. The targets of these proteases include the nuclear enzymes poly(adenosine diphosphate[ADP]-ribose) polymerase (PARP) and DNA-dependent protein kinase (DNA-PK), both involved in aspects of DNA damage sensing and repair. Additional targets are U1 small nuclear ribonucleoprotein and the nuclear lamins (lamins A, B1/B2, and C), and, in the cytoplasm, Gas2, a component of the microfilament system, protein kinase Cδ (PKCδ) and various components of the cytoskeleton, such as actin and the sterol regulatory element-binding proteins SREBP-1 and SREBP-2 [120,121]. ICE and CPP32 are highly selective in their proteolytic activity [122–127]. A series of peptide analogue substrates has elucidated the role of these proteases in the programmed cell death process. It has been shown that ICE cleaves a sequence composed by the tetrapep-tide YVAD, whereas CPP32 cleaves a DEVD sequence (Figure 3).
Protein Kinase C-Delta Defect in Autoimmune Lymphoproliferative Syndrome-Like Disease: First Case from the National Iranian Registry and Review of the Literature
Published in Immunological Investigations, 2022
Niusha Sharifinejad, Gholamreza Azizi, Nasrin Behniafard, Majid Zaki-Dizaji, Mahnaz Jamee, Reza Yazdani, Hassan Abolhassani, Asghar Aghamohammadi
Recently, patients homozygous for a null mutation in the gene that encodes Protein kinase C delta PRKCδ (PRKCD), display some features of the ALPS, including autoimmunity, neutropenia, increased B-cell numbers and proliferation, with diminished NK cell function, making PRKCδ an appealing candidate gene for ALPS-like disease (Salzer et al. 2013). PRKC is a family of serine/threonine kinases that play a key role in the regulation of various cellular processes. It contributes to both B- and T-cell signaling, as well as regulation of growth, apoptosis, and differentiation of a variety of cell types (Guo et al. 2004; Limnander et al. 2011). The impressive lymphocyte accumulation seen in these patients could be explained by the excessive proliferation of the patient’s B cells demonstrated ex vivo, as well as by defective B cell apoptosis (Guo et al. 2004; Limnander et al. 2011).
New and emerging drug therapies for Cushing’s disease
Published in Expert Opinion on Pharmacotherapy, 2018
Sylvère Störmann, Jochen Schopohl
Protein kinase C delta (PRKCD) is a serine-threonine kinase that regulates proliferation, cell cycle, differentiation, and apoptosis [134]. PRKCD levels are low in corticotroph adenomas [135]. In a recent study, PRKCD was silenced in a murine corticotroph cell line which led to increased cell viability, enhanced POMC/ACTH expression, morphological changes associated with deregulation of adhesion molecules, upregulated EGFR expression, and sensitivity to anti-EGFR molecules [136]. This led to the hypothesis that PRKCD restrains ACTH-secreting pituitary cells from acquiring aggressive behavior.
Immunologic evaluation and genetic defects of apoptosis in patients with autoimmune lymphoproliferative syndrome (ALPS)
Published in Critical Reviews in Clinical Laboratory Sciences, 2021
Laura Casamayor-Polo, Marta López-Nevado, Estela Paz-Artal, Alberto Anel, Frederic Rieux-Laucat, Luis M. Allende
Protein kinase C delta (PRKCD) deficiency or ALPS-III (OMIM 615559) is a disorder of immune dysregulation caused by AR mutations in the PRKCD gene. Patients show a variable phenotype that is characterized mainly by lymphadenopathy, lupus-like autoimmunity, chronic EBV infection, and other recurrent infections. Immunological studies show memory B cell lymphopenia and hypogammaglobulinemia [79].