Interaction of ATF6 and serum response factor

Zhu, Cheng; Johansen, Finn–Eirik; Prywes, Ron

doi:10.1128/mcb.17.9.4957

Cited by 151 publications

(148 citation statements)

References 30 publications

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“…The recent discovery that a new ATF family member, ATF6, which is present in the heart, binds to SRF and participates in SRF/SRE-enhanced transcription in response to serum (19), led us to evaluate whether ATF6 might serve as a convergence point for p38. When studied in vitro, ATF6 was phosphorylated by p38, while SRF was not.…”

Section: Discussionmentioning

confidence: 99%

“…Accordingly, the possibility that p38, or a downstream kinase, might phosphorylate a non-Ets-related SRF-binding partner was considered. One such protein is ATF6, a 670-amino acid member of the b-ZIP, ATF/CREB family recently shown to bind SRF, but not SREs, and to enhance SRF-mediated transcription (19). Interestingly, when ATF6 was incubated with p38 it was phosphorylated (Fig.…”

Section: Mapping P38-inducible Elements In the Anf Promoter-tomentioning

confidence: 99%

“…This construct has previously been used in HeLa cells to demonstrate the dependence of serum activation of SRF on ATF6 (19). Myocardial cells were co-transfected with MKK6 (Glu), various levels of the ATF6 antisense construct, and ANF 65 (ANF SRE).…”

Section: Mapping P38-inducible Elements In the Anf Promoter-tomentioning

confidence: 99%

“…Primary myocardial cells were transfected with ANF 65 (ANF SRE), SV40-␤-galactosidase, Ϯ MKK6 (Glu), Ϯ various levels of ATF6-AS, the latter of which codes for an antisense form of the ATF6 (19). Cultures were maintained for 48 h in serum-free media and then the cells were extracted, analyzed for reporter enzyme activity, and the results plotted as described in the legend to Fig.…”

Section: Fig 4 Effects Of Antisense Atf6 On Anf Promoter Activitymentioning

confidence: 99%

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p38 Mitogen-activated Protein Kinase Mediates the Transcriptional Induction of the Atrial Natriuretic Factor Gene through a Serum Response Element

Thuerauf

Arnold

Zechner

et al. 1998

Journal of Biological Chemistry

117

100

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In various cell types certain stresses can stimulate p38 mitogen-activated protein kinase (p38 MAPK), leading to the transcriptional activation of genes that contribute to appropriate compensatory responses. In this report the mechanism of p38-activated transcription was studied in cardiac myocytes where this MAPK is a key regulator of the cell growth and the cardiac-specific gene induction that occurs in response to potentially stressful stimuli. In the cardiac atrial natriuretic factor (ANF) gene, a promoter-proximal serum response element (SRE), which binds serum response factor (SRF), was shown to be critical for ANF induction in primary cardiac myocytes transfected with the selective p38 MAPK activator, MKK6 (Glu). This ANF SRE does not possess sequences typically required for the binding of the Ets-related ternary complex factors (TCFs), such as Elk-1, indicating that p38-mediated induction through this element may take place independently of such TCFs. Although p38 did not phosphorylate SRF in vitro, it efficiently phosphorylated ATF6, a newly discovered SRF-binding protein that is believed to serve as a coactivator of SRF-inducible transcription at SREs. Expression of an ATF6 antisense RNA blocked p38-mediated ANF induction through the ANF SRE. Moreover, when fused to the Gal4 DNA-binding domain, an N-terminal 273-amino acid fragment of ATF6 was sufficient to support trans-activation of Gal4/luciferase expression in response to p38 but not the other stress kinase, Nterminal Jun kinase (JNK); p38-activating cardiac growth promoters also stimulated ATF6 trans-activation. These results indicate that through ATF6, p38 can augment SRE-mediated transcription independently of Ets-related TCFs, representing a novel mechanism of SRF-dependent transcription by MAP kinases.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Mapping P38-inducible Elements In the Anf Promoter-tomentioning

confidence: 99%

Section: Mapping P38-inducible Elements In the Anf Promoter-tomentioning

confidence: 99%

Section: Fig 4 Effects Of Antisense Atf6 On Anf Promoter Activitymentioning

confidence: 99%

See 2 more Smart Citations

p38 Mitogen-activated Protein Kinase Mediates the Transcriptional Induction of the Atrial Natriuretic Factor Gene through a Serum Response Element

Thuerauf

Arnold

Zechner

et al. 1998

Journal of Biological Chemistry

117

100

View full text Add to dashboard Cite

show abstract

“…Among the transcription factors that influence SRF activity are Ying Yang 1 (YY1) (14), the homeodomain proteins phox1/ MHox (15,16) and Nkx2.5 (9), NF-B (17), ATF6 (18), myogenic basic helix loop helix factors (19), and members of the ETS family of proto-oncogene products (reviewed in Ref. 20).…”

mentioning

confidence: 99%

Cooperative Transcriptional Activation by Serum Response Factor and the High Mobility Group Protein SSRP1

Spencer¹,

Baron²,

Olson³

1999

Journal of Biological Chemistry

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Serum response factor (SRF) is a MADS box transcription factor that controls a wide range of genes involved in cell proliferation and differentiation. The MADS box mediates homodimerization and binding of SRF to the consensus sequence CC(A/T) 6 GG, known as a CArG box, which is found in the control regions of numerous serum-inducible and muscle-specific genes. Using a modified yeast one-hybrid screen to identify potential SRF cofactors, we found that SRF interacts with the high mobility group factor SSRP1 (structure-specific recognition protein). This interaction, which occurs in yeast and mammalian cells, is mediated through the MADS box of SRF and a basic region of SSRP1 encompassing amino acids 489 -542, immediately adjacent to the high mobility group domain. SSRP1 does not bind the CArG box, but interaction of SSRP1 with SRF dramatically increases the DNA binding activity of SRF, resulting in synergistic transcriptional activation of native and artificial SRF-dependent promoters. These results reveal an important role for SSRP1 as a coregulator of SRF-dependent transcription in mammalian cells.

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Endoplasmic reticulum stress triggers an acute proteasome‐dependent degradation of ATF6

Hong

Mao

et al. 2004

J of Cellular Biochemistry

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ATF6, a 670 amino acid endoplasmic reticulum (ER) transmembrane glycoprotein with the electrophoretic mobility of a 90 kDa protein, is a key transcriptional activator of the unfolded protein response (UPR) that allows mammalian cells to maintain cellular homeostasis when the cells are subjected to a variety of environmental and physiological stress. Previous studies have established that ATF6 is a short-lived protein, the activation of which involves relocation from the ER to the Golgi where it is cleaved by the S1P/S2P protease system to generate a nuclear form that acts as a transcriptional activator for ER-stress inducible target genes such as Grp78/BiP. We report here that in addition to this process, ER-stress mediated by thapsigargin triggers an acute proteasomal degradation of the pre-existing pool of p90ATF6 independent of S1P/S2P cleavage. We showed that ATF6 is a direct target of proteasome-ubiquitin pathway, and this process can be suppressed by proteasome inhibitors, ALLN and MG115. We further observed that in non-stressed cells, p90ATF6 can be stabilized by MG115 but not ALLN and that treatment of cells with MG115 results in Grp78 induction in the absence of ER stress. These studies suggest that ER-stress induced acute, transit degradation of p90ATF6 could represent a novel cellular defense mechanism to prevent premature cell death resulting from p90ATF6 activation. Further, inhibition of proteasome activity can result in chaperone protein gene induction through stabilization of p90ATF6 as well as accumulation of malfolded proteins.

show abstract

Interaction of ATF6 and serum response factor

Cited by 151 publications

References 30 publications

p38 Mitogen-activated Protein Kinase Mediates the Transcriptional Induction of the Atrial Natriuretic Factor Gene through a Serum Response Element

p38 Mitogen-activated Protein Kinase Mediates the Transcriptional Induction of the Atrial Natriuretic Factor Gene through a Serum Response Element

Cooperative Transcriptional Activation by Serum Response Factor and the High Mobility Group Protein SSRP1

Endoplasmic reticulum stress triggers an acute proteasome‐dependent degradation of ATF6

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