PI3K cat class IA (p110-beta), G-protein alpha-0, PKC-epsilon, PLC-beta1, PI3K reg class IA (p85-alpha), SOS1, c-Raf-1, 126.96.36.199, PKC-delta, PKC-alpha, CaMK II, Ca('2) cytosol, TGM2, Ca('2+) endoplasmic reticulum, G-protein alpha-q, MEK1(MAP2K1), 188.8.131.52, MEK2(MAP2K2), Alpha-1A adrenergic receptor, c-Src, IP3, Noradrenaline extracellular region, PLC-delta 1, H-Ras, c-Fos, Adrenaline extracellular region, IP3 receptor, G-protein alpha-14, G-protein beta/gamma, L-type Ca(II) channel, alpha 1C subunit, PtdIns(3,4,5)P3, PtdIns(4,5)P2, G-protein alpha-11, Alpha-1B adrenergic receptor, Shc, G-protein alpha-15, c-Jun, Pyk2(FAK2), Erk (MAPK1/3), Alpha-1D adrenergic receptor, DAG, Ca('2+) extracellular region, None, None, Calmodulin
Activation of ERK by Alpha-1 adrenergic receptors
Subtype alpha-1 adrenergic receptors consists of Alpha-1A adrenergic receptor, Alpha-1B adrenergic receptor and Alpha-1D adrenergic receptor. They participate in many physiological processes via different pathways. One of the best studied alpha-1 adrenergic receptors-stimulated pathways is a Mitogen-activated protein kinase 1 and 3 ( ERK1/2 ) activation , .
Natural catecholamines, Adrenaline, and Noradrenaline, activate alpha-1 adrenergic receptors , . The activated receptors interact with different Guanine nucleotide binding proteins (G-proteins). All three receptors interact with G-protein alpha-q and G-protein alpha-11 . Alpha-1A adrenergic receptor and Alpha-1B adrenergic receptor couple with G-protein alpha-14 . Alpha-1B adrenergic receptor and Alpha-1D adrenergic receptor interact with Transglutaminase 2 ( TGM2 ) , , . Alpha-1B adrenergic receptor couples with G-protein alpha-15  and G-protein alpha activating activity polypeptide O ( G-protein alpha-o ) .
G-protein alpha-11, G-protein alpha-q, G-protein alpha-14, G-protein alpha-15 activate Phospholipase C beta 1 ( PLC-beta1 ) , , . TGM2 activate Phospholipase C delta 1 ( PLC-delta1 ) , . PLC-beta1 and PLC-delta1 hydrolyze Phosphatidylinositol-4,5-bisphosphate ( PtdIns(4,5)P2 ) to produce Inositol 1,4,5-trisphosphate ( IP3 ) and 1,2-diacyl-glycerol ( DAG ) , .
DAG and IP3 participate in activation of Ca('2+) -dependent Protein kinase C alpha ( PKC-alpha ) , Ca('2+) -independent Protein kinases C delta and epsilon ( PKC-delta and PKC-epsilon ) , ,  and mobilization of intracellular Ca('2+). All these pathways may lead to activation of cell growth and proliferation.
Cytosolic Ca('2+) activates Calmodulin/ Calcium/calmodulin-dependent protein kinase II ( CaMK II )/ PTK2B protein tyrosine kinase 2 beta ( Pyk2(FAK2) )/ v-src sarcoma viral oncogene homolog ( c-Src )/ SHC transforming protein ( Shc )/ Son of sevenless homolog ( SOS )/ v-Ha-ras Harvey rat sarcoma viral oncogene homolog ( H-Ras )/ v-raf-1 murine leukemia viral oncogene homolog 1 ( c-Raf-1 )/ Mitogen-activated protein kinase kinases 1 and 2 (( MEK1(MAP2K1) and MEK2(MAP2K2) )/ Mitogen-activated protein kinase 1 and 3 ( ERK1/2 ) pathway , .
G-protein alpha-q -stimulated PKC-alpha and PKC-epsilon may activate Erk cascade in H-Ras -independent manner (e.g., via phosphorylation of c-Raf-1) , . On the other hand PKC-delta and PKC-epsilon may activate Erk cascade in H-Ras -independent manner via phosphorylation of Pyk2(FAK2) , , .
Alpha-1 adrenergic receptors-dependent ERK1/2 activation may also be realized via Phosphoinositide-3-kinase ( PI3K ) , . c-Src can activate PI3K reg class IA (p85-alpha)/ PI3K cat class IA (p110-beta) directly , ,  or via SHC transforming protein ( Shc )/ Son of sevenless homolog ( SOS )/ H-Ras .
Activated PI3K catalyzes transformation of PtdIns(4,5)P2 in to Phosphatidylinositol-3,4,5-trisphosphate ( PtdIns(3,4,5)P3 ). Presumably, then PtdIns(3,4,5)P3 activates Shc/ SOS/ H-Ras. After that, H-Ras activates c-Raf-1/ MEK1(MAP2K1), MEK2(MAP2K2) )/ ERK1/2 , , .
Moreover, PKC-alpha, probably phosphorylates Ca2+ channels (for example, Calcium channel, voltage-dependent L type ( L-type Ca(II) channel ) ,  ) and this increase extracellular Ca('2+) entry . High level of Ca('2+) influence cell contraction . Also, high level of Ca('2+), which was achieved due Ca2+ channels activation, may facilitate activation of Ca('2+) -dependent PKC-alpha, thus creating a positive feedback loop. CaMK II may activates L-type Ca(II) channel as well .