Search results for PRKCD

Showing 14 results out of 19

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Protein (7 results from a total of 12)

Identifier: R-HSA-58200
Species: Homo sapiens
Compartment: cytosol
Primary external reference: UniProt: Q05655
Identifier: R-HSA-212547
Species: Homo sapiens
Compartment: cytosol
Primary external reference: UniProt: PRKCD: Q05655
Identifier: R-HSA-6806226
Species: Homo sapiens
Compartment: extracellular region
Primary external reference: UniProt: PRKCD: Q05655
Identifier: R-HSA-450606
Species: Homo sapiens
Compartment: nucleoplasm
Primary external reference: UniProt: PRKCD: Q05655
Identifier: R-HSA-5218746
Species: Homo sapiens
Compartment: cytosol
Primary external reference: UniProt: PRKCD: Q05655
Identifier: R-HSA-6799221
Species: Homo sapiens
Compartment: azurophil granule lumen
Primary external reference: UniProt: PRKCD: Q05655
Identifier: R-HSA-5607635
Species: Homo sapiens
Compartment: plasma membrane
Primary external reference: UniProt: PRKCD: Q05655

Set (1 results from a total of 1)

Identifier: R-HSA-8934444
Species: Homo sapiens
Compartment: plasma membrane

Complex (2 results from a total of 2)

Identifier: R-HSA-5607689
Species: Homo sapiens
Compartment: plasma membrane
Identifier: R-HSA-5607700
Species: Homo sapiens
Compartment: plasma membrane

Reaction (4 results from a total of 4)

Identifier: R-HSA-5607734
Species: Homo sapiens
Compartment: plasma membrane, cytosol
Protein kinase C-delta (PRKCD), activated upon CLEC7A (Dectin-1)-SYK signaling, phosphorylates CARD9 leading to NF-kB activation (Strasser et al. 2012) and complex formation between CARD9 and BCL10. CLEC6A (Dectin-2) and CLEC4E (Mincle) also induces intracellular signaling through PRKCD and CARD9-BCL10-MALT1 pathway. Similar to the CLEC7A responses, both CLEC6A and CLEC4E-induced interleukin 10 (IL10) and tumour necrotic factor (TNF) production were severely impaired in the absence of PRKCD (Strasser et al. 2012). PRKCD is a member of the Ca2+ independent and diacylglycerol (DAG) dependent novel PKC subfamily. PKC family members exist in an immature inactive conformation that requires post-translational modifications to achieve catalytic maturity. The catalytic maturation of PRKCD involves the auto-phosphorylation of Ser645 and the phosphorylation of Thr507 and Ser664 (Li et al. 1997, Keranen et al. 1995). These phosphorylations of activation loop residues act as a priming step that allows the catalytic maturation of PRKCD (Dutil et al. 1998). Fully phosphorylated and primed PRKCD localises to the cytosol with its pseudosubstrate occupying the substrate-binding cavity. Signals that cause the lipid hydrolysis recruit PKC to membranes. The C1 domain in PRKCD is a cysteine-rich compact structure, identified as the interaction site for DAG and phorbol ester. PRKCD preferentially translocates to the plasma membrane (Stahelin et al. 2004, Newton 2010).
Identifier: R-HSA-8934446
Species: Homo sapiens
Compartment: cytosol, plasma membrane
Activated protein kinase C alpha (PRKCA), as well as delta (PRKCD) and epsilon (PRKCE), can phosphorylate SHC1 splicing isoforms SHC1-1 (p66Shc) and SHC1-2 (p52Shc) on serine residues S139 and S29, respectively (Habib et al. 1994, Faisal et al. 2002).
Identifier: R-HSA-6787820
Species: Homo sapiens
Compartment: plasma membrane, extracellular region
The receptor for Interleukin-34 (IL34) is colony stimulating factor 1 receptor (CSF1R), also called macrophage colony stimulating factor receptor (M-CSF-R). Dimeric IL34 and CSF1 bind the same general region of CSF1R, interacting with overlapping but distinct epitopes. Ligand binding leads to receptor dimerisation (Ma et al. 2012, Liu et al. 2012). Like CSF1, IL34 stimulation of CSF1R leads to phosphorylation of extracellular signal-regulated kinase (ERK) 1 and 2 in human monocytes (Lin et al. 2008). CSF1R activates several signaling pathways including JAK-STAT3, 5A/B, phosphorylation of PIK3R1, PLCG2, GRB2, SLA2 and CBL. PLCG2 phosphorylation leads to increassed production of the cellular signaling molecules diacylglycerol (DAG) and inositol 1,4,5 trisphosphate (IP3), which activate protein kinase C family members, especially PRKCD. Phosphorylation of PIK3R1, the regulatory subunit of phosphatidylinositol 3 kinase, leads to activation of the AKT1 signaling pathway. Activated CSF1R also mediates activation of MAPK1 (ERK2) or MAPK3 (ERK1) and the SRC family kinases SRC, FYN and YES1. Activated CSF1R binds GRB2 and promotes tyrosine phosphorylation of SHC1 and INPP5D (SHIP1). Signaling is down regulated by protein phosphatases such as INPP5D that can dephosphorylate the receptor and its downstream effectors.
Identifier: R-HSA-5607740
Species: Homo sapiens
Compartment: plasma membrane, cytosol
Activation of NF-kB signaling is a critical event downstream of CLEC7A (Dectin-1), CLEC6A (Dectin-2) (Bi et al. 2010) and CLEC4E (Mincle) (Yamasaki et al. 2008), requiring the adapter protein Caspase recruitment domain (CARD)-containing protein 9 (CARD9) in dendritic cells and in macrophages (Gross et al. 2006, Hara et al. 2007). CARD9 is analogous to CARD-containing MAGUK protein 1 (CARMA1), which mediates T-cell receptor (TCR) activation of NF-kB in lymphocytes. CARD9 is downstream of SYK and becomes phosphorylated by PRKCD (Protein kinase C-delta) phosphorylates CARD9 on Thr-231 (T231), which is required for the signal-induced association of CARD9 with B-cell lymphoma 10 (BCL10) and Mucosa-associated lymphoid tissue 1 (MALT1) and the subsequent recruitment of MAP3K transforming growth factor beta activated kinase 1 (TAK1), leading to activation of the NF-kB pathway (Strasser et al. 2012). A homozygous loss-of-function mutation in human CARD9 results in a premature termination codon (Gln295*). Patients with this mutation are highly susceptible to fungal infections (Glocker et al. 2009).
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