polyclonal

(Widmer et al., 2018, Fropf et al., 2013, Tubon et al., 2013, Zhang et al., 2013)

monoclonal

(Hirano et al., 2016, Belvin et al., 1999)

Source for merge of: CrebB-17A l(1)17Af

(Belvin et al., 1999)

Source for merge of: CrebB-17A CrebB-17B

(FlyBase, 1992-)

Expression is affected in Fmr1 mutants.

(Dockendorff et al., 2002)

Cycling CrebB-17A activity is abolished in a per mutant, indicating that CrebB-17A and per affect each other and may participate in the same regulatory feedback loop.

(Belvin et al., 1999)

Mutation in CrebB-17A shortens circadian locomotor rhythms and dampens the oscillations of per.

(Belvin et al., 1999)

CrebB-17A supports cycling of the per/tim oscillator.

(Belvin et al., 1999)

CrebB-17A binds to the Ubx cAMP response element (CRE), located in an enhancer, and ubiquitous expression of a dominant negative form of CrebB-17A suppresses CRE-mediated reporter gene expression and reduces lab expression in the endoderm.

(Eresh et al., 1997)

CrebB-17A acts in parallel with Fas2 to cause an increase in synaptic strength. cAMP initiates these parallel changes to achieve long-term synaptic enhancement. Expression of the CrebB-17A repressor in the dnc mutant blocks functional but not structural plasticity. Expression of the CrebB-17A activator increases synaptic strength, but only in Fas2 mutants that increase bouton number, due to increased presynaptic transmitter release. Expression of CrebB-17A in a Fas2 mutant background genetically reconstitutes cAMP-dependent plasticity. Thus, cAMP initiates parallel changes in CrebB-17A and Fas2 to achieve long-term synaptic enhancement.

(Davis et al., 1996)

Long term memory formation can be prevented by an inducible repressor form of CrebB-17A.

(Tully, 1995)

Long term memory (LTM) is blocked specifically by induced expression of a repressor isoform of CrebB-17A. LTM formation is enhanced after induced expression of an activator form of CrebB-17A. LTM formation depends on phosphorylation of the CrebB-17A product. FlyBase curator comment: see FBrf0180428 for re-examination of these conclusions in light of discovery that CrebB-17A^a.hs actually encodes a mutant form of CrebB-17A isoform a. In contrast to results reported in FBrf0080505, FBrf0180428 reports that heat shock of CrebB-17A^a.hs was found to exert no effect on LTM in 1x training session - though assay was carried out at 5, as opposed to 7 days. CrebB-17A^b.hs, however, does have an effect on LTM.

(Yin et al., 1995)

CrebB-17A has been cloned and sequenced.

(Yin et al., 1995)

Over-expression of the b isoform of CrebB-17A completely blocks long-term memory, but leaves anaesthesia resistant memory and learning unaffected.

(Yin et al., 1994)

The structure of CrebB-17A is reminiscent of genes in the mammalian CREB family.

(Usui et al., 1993)