Membrane depolarization and calcium influx stimulate MEK and MAP kinase via activation of Ras

Rosen, Laura; Ginty, David D.; Weber, Michael J.; Greenberg, Michael E.

doi:10.1016/0896-6273(94)90438-3

Cited by 654 publications

(480 citation statements)

References 94 publications

Supporting

Mentioning

436

Contrasting

Unclassified

Order By: Relevance

“…The release of intracellular Ca 2ϩ stores can activate and modulate several pathways important in mediating cell attachment, spreading, and cell migration (Rosen et al, 1994;Farnsworth et al, 1995;Rosen and Greenberg, 1996;Price et al, 2003;Jin et al, 2005;Lebart and Benyamin, 2006). Because Hcys' effects on cardiac NC cell attachment were substrate specific, Hcys-induced Ca 2ϩ release may have altered integrin binding and/or signaling activity.…”

Section: Discussionmentioning

confidence: 99%

Homocysteine enhances cardiac neural crest cell attachment in vitro by increasing intracellular calcium levels

Heidenreich

Reedy

Brauer

2008

Developmental Dynamics

View full text Add to dashboard Cite

Elevated homocysteine (Hcys) increases the risk of neurocristopathies. Previous studies show Hcys inhibits neural crest (NC) cell migration in vivo. However, the mechanisms responsible for this effect are unknown. Here, we evaluated the effect of Hcys on NC cell attachment in vitro and determined if any of the effects were due to altered Ca 2؉ signaling. We found Hcys enhanced NC cell attachment in a dose and substratedependent manner. Ionomycin mimicked the effect of Hcys while BAPTA-AM and 2-APB blocked the effect of Hcys on NC attachment. In contrast, inhibitors of plasma membrane Ca 2؉ channels had no effect on NC attachment. Hcys also increased the emission of the intracellular Ca 2؉ -sensitive probe, Fluo-4. These results show Hcys alters NC attachment by triggering an increase in intracellular Ca 2؉ possibly by generating inositol triphosphate. Hence, the teratogenic effect ascribed to Hcys may be due to perturbation of intracellular Ca 2؉ signaling.

show abstract

Section: Discussionmentioning

confidence: 99%

Homocysteine enhances cardiac neural crest cell attachment in vitro by increasing intracellular calcium levels

Heidenreich

Reedy

Brauer

2008

Developmental Dynamics

View full text Add to dashboard Cite

show abstract

“…In these mutants the abnormal calcium signaling could involve processes other than neurotransmitter release (Ghosh & Greenberg, 1995). For example, calcium influx can activate intracellular pathways, which can act locally at the synapse or mediate changes in nuclear gene transcription (Rosen et al, 1994;Ghosh & Greenberg, 1995;Curtis & Finkbeiner, 1999), processes that have the potential to alter cell surface molecules that may be critical to normal synapse formation. In vitro studies have presented a possible link between VDCCs and photoreceptor development in which VDCC blockade inhibits process outgrowth, varicosity formation, and vesicle protein synthesis in developing rods (Zhang & Townes-Anderson, 2002;NachmanClewner et al, 1999).…”

Section: Role Of the α 1f Subunit Of The Vdcc In Synaptic Developmentmentioning

confidence: 99%

Thenob2mouse, a null mutation inCacna1f: Anatomical and functional abnormalities in the outer retina and their consequences on ganglion cell visual responses

et al. 2006

View full text Add to dashboard Cite

Glutamate release from photoreceptor terminals is controlled by voltage-dependent calcium channels (VDCCs). In humans, mutations in the Cacna1f gene, encoding the α 1F subunit of VDCCs, underlie the incomplete form of X-linked congenital stationary night blindness (CSNB2). These mutations impair synaptic transmission from rod and cone photoreceptors to bipolar cells. Here, we report anatomical and functional characterizations of the retina in the nob2 (no b-wave 2) mouse, a naturally occurring mutant caused by a null mutation in Cacna1f. Not surprisingly, the b-waves of both the light-and dark-adapted electroretinogram are abnormal in nob2 mice. The outer plexiform layer (OPL) is disorganized, with extension of ectopic neurites through the outer nuclear layer that originate from rod bipolar and horizontal cells, but not from hyperpolarizing bipolar cells. These ectopic neurites continue to express mGluR6, which is frequently associated with profiles that label with the

show abstract

“…In neuroendocrine PC12 cells, Ca 2+ transients alone are su cient to trigger ERK activation (Rosen et al, 1994). Therefore, we tested whether an increase in [Ca 2+ ] i would su ce to stimulate ERK activity in H69 cells.…”

Section: Activation Of Extracellular Signal-regulated Kinasesmentioning

confidence: 99%

The galanin receptor type 2 initiates multiple signaling pathways in small cell lung cancer cells by coupling to Gq, Gi and G12 proteins

et al. 2000

View full text Add to dashboard Cite

Neuropeptides like galanin produced and released by small cell lung cancer (SCLC) cells are considered principal mitogens in these tumors. We identi®ed the galanin receptor type 2 (GALR2) as the only galanin receptor expressed in H69 and H510 cells. Photoa nity labeling of G proteins in H69 cell membranes revealed that GALR2 activates G proteins of three subfamilies: G q , G i , and G 12 . In H69 cells, galanin-induced Ca 2+ mobilization was pertussis toxin-insensitive. While phorbol ester-induced extracellular signal-regulated kinase (ERK) activation required protein kinase C (PKC) activity, preincubation of H69 cells with the PKCinhibitor GF109203X had no e ect on galanin-dependent ERK activity. A rise of the intracellular calcium concentration was necessary and su cient to mediate galanin-induced ERK activation. In support of G i coupling, stimulation of GALR2 expressed in HEK293 cells inhibited isoproterenol-induced cAMP accumulation and raised cAMP levels in COS-7 cells when coexpressed with a chimeric Ga S -Ga i protein. In H69 cells, galanin activated the monomeric GTPase RhoA and induced stress ®ber formation in Swiss 3T3 cells expressing GALR2. Thus, we provide the ®rst direct evidence that in SCLC the mitogenic neuropeptide galanin, interacting with GALR2, simultaneously activates multiple classes of G proteins and signals through the G q phospholipase C/calcium sequence and a G 12 /Rho pathway. Oncogene (2000) 19, 4199 ± 4209.

show abstract

Membrane depolarization and calcium influx stimulate MEK and MAP kinase via activation of Ras

Cited by 654 publications

References 94 publications

Homocysteine enhances cardiac neural crest cell attachment in vitro by increasing intracellular calcium levels

Homocysteine enhances cardiac neural crest cell attachment in vitro by increasing intracellular calcium levels

Thenob2mouse, a null mutation inCacna1f: Anatomical and functional abnormalities in the outer retina and their consequences on ganglion cell visual responses

The galanin receptor type 2 initiates multiple signaling pathways in small cell lung cancer cells by coupling to Gq, Gi and G12 proteins

Contact Info

Product

Resources

About