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phosphosite cbn pc11 biopax bel_lc signor biogrid lincs_drug tas hprd trrust ctd virhostnet phosphoelm drugbank omnipath | geneways tees isi trips rlimsp medscan sparser eidos reach
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"We further show that BEC-1 and Beclin1 acts independently of the GLP-1 and Notch or DAF-7 and TGFbeta pathways, but together with the DAF-2 and insulin IGF-1 receptor (IIR) signaling pathway to promote germline stem cell proliferation."
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"In contrast, loss of BEC-1 function further decreased germ cell proliferation in the glp-1 (e2141lf) loss-of-function allele, which is characterized by a reduction in germline progenitors and a severe Glp (abnormal germline proliferation) phenotype, where germ cells do not proliferate and differentiate prematurely [19]."
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"We found that BEC-1 expression from a hypodermal [Pdpy-7 : : BEC-1], a muscle specific [Pmyo-3 : : BEC-1], its own promoter [Pbec-1 : : BEC-1], and less so from a pan-neuronal promoter [Prgef-1 : : BEC-1], rescued the germline proliferation defects in bec-1 mutant animals (XREF_FIG, XREF_SUPPLEMENTARY)."
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"We conclude that bec-1 acts in a pathway with daf-2 and IIR signaling to promote germline proliferation."
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"Taken together, our glp-1 and Notch gain and loss of function experiments suggest that BEC-1 and Beclin1 functions, at least in part, independently of GLP-1 and Notch activity to promote germ cell proliferation."
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"In contrast, expression of bec-1 from an intestinal promoter [P glo-1 : : BEC-1] did not rescue the proliferation defect of bec-1 mutants."
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"BEC-1 functions in a DAF-18 and PTEN and SKN-1 and Nrf dependent but DAF-16 and FOXO independent manner to promote germline proliferation."
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"In contrast, expression of bec-1 from an intestinal promoter [Pglo-1 : : BEC-1] did not rescue the proliferation defect of bec-1 mutants (XREF_FIG)."
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"BEC-1 and Beclin1 promotes germline stem cell proliferation cell non autonomously from somatic tissues."
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"In contrast, loss of BEC-1 function further decreased germ cell proliferation in the glp-1 (e2141lf) loss of function allele (XREF_SUPPLEMENTARY), which is characterized by a reduction in germline progenitors, and a severe Glp (Germline abnormal proliferation) phenotype, where germ cells do not proliferate and differentiate prematurely [XREF_BIBR]."
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"Taken together, our glp-1 and Notch gain- and loss-of-function experiments suggest that BEC-1 and Beclin1 functions, at least in part, independently of GLP-1 and Notch activity to promote germ cell proliferation.The reduction of germline proliferation in autophagy mutants is similar to that of loss-of-function mutants in daf-2 / IIR signaling [14]."
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"Interestingly, tissue specific overexpression of bec-1 in neurons, muscles, and intestine in wild-type animals also decreased proliferation."
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"Interestingly, tissue specific over-expression of bec-1 in neurons, muscles and intestine in wild-type animals also decreased proliferation (XREF_FIG)."
Ced-9 affects KCNH3
| 2 5
| 2 5
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"Furthermore, BEC-1 forms a complex with the antiapoptotic protein CED-9 and Bcl-2, and its depletion triggers CED-3 and Caspase-dependent PCD."
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"Because this regulatory mechanism is probably evolutionary conserved in C. elegans [XREF_BIBR, XREF_BIBR], it could be the case that DAPK-1 modulates autophagy by regulating the interaction between BEC-1 and CED-9 in C. elegans."
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"The interaction between Beclin-1 and pro survival Bcl-2, used to inhibit autophagy, is conserved in the nematode model, with BEC-1 and CED-9 protein interactions disrupting the formation of the Beclin-1 initiation complex."
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"Because this regulatory mechanism is probably evolutionary conserved in C. elegans [ xref , xref ], it could be the case that DAPK-1 modulates autophagy by regulating the interaction between BEC-1 and CED-9 in C. elegans ."
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"It is possible that DAPK-1 and JNK-1 modulate autophagy by regulating the interaction between BEC-1 and CED-9 in a tissue-specific manner."
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"Thus, EGL-1 might not only positively regulate programmed cell death, but might also positively regulate autophagy by interacting with CED-9 to induce BEC-1 release from CED-9 and BEC-1 complexes."
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"It is possible that DAPK-1 and JNK-1 modulate autophagy by regulating the interaction between BEC-1 and CED-9 in a tissue specific manner."
FOXG1 affects KCNH3
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FOXG1 increases the amount of KCNH3. 6 / 6
| 6
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"FOXG1 activates Kcnh3 transcription."
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"Our finding that FOXG1 increases expression of Kcnh3 extends the view that FOXG1 has important functions in mature neurons beyond integration of pyramidal neurons into the cortical plate."
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"Our observation that FOXG1 increases Kcnh3 expression may also bear clinical relevance, as knockout mice for Kcnh3 show improved cognitive performance, enhanced spatial working memory and enhanced latent learning memory [XREF_BIBR]."
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"We concluded that Kcnh3 expression is increased by FOXG1 and FOXO3, but is independent of FOXO1 and TGFbeta signaling."
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"In mature neurons, FOXG1 activates transcription of the seizure related Kcnh3, which might be a FOXG1-target gene involved in the FOXG1 syndrome pathology."
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"In contrast to its repressive function in Cdkn1a transcription, FOXG1 activated Kcnh3 transcription."
KCNH3 affects autophagy
| 5
KCNH3 activates autophagy.
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| 4
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"NAF-1 is a component of the inositol-1,4,5 trisphosphate (IP3) receptor complex, which contributes to the interaction of Bcl-2 with Bec1 and is required for Bcl-2 to functionally antagonize Bec1 mediated autophagy."
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"Alternatively, other functions of bec-1, such as endosome-to-Golgi retrograde transport, may be required to support long life, rather than autophagy."
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"Indeed, the initial step of autophagy, mediated by BEC-1 (Atg6, Homolog of Beclin-1) is crucial to correct dauer formation."
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"Accordingly, the longevity extending effects of PNC-1 were lost upon the knockdown of SIR-2.1, as well as upon that of either of the two essential autophagy modulators BEC-1 or ATG-5 [XREF_BIBR]."
KCNH3 inhibits autophagy.
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| 1
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"Moreover, loss of bec-1 resulted in a decline in lipid levels in daf-2 [insulin and IGF -1 receptor (IIR) ortholog] mutants and in germline-less glp-1 and Notch animals, both previously recognized to accumulate neutral lipids and have increased autophagy levels."
KCNH3 affects GCG
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KCNH3 inhibits GCG.
| 3
KCNH3 inhibits GCG. 3 / 3
| 3
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"In contrast, loss of BEC-1 function further decreased germ cell proliferation in the glp-1 (e2141lf) loss-of-function allele, which is characterized by a reduction in germline progenitors and a severe Glp (abnormal germline proliferation) phenotype, where germ cells do not proliferate and differentiate prematurely [19]."
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"However, we found that bec-1 and beclin1 RNAi still reduced the number of mitotic germ cells in the gld-2 (q497) gld-1 (q1485); glp-1 (q175) triple mutants to an extent similar to that in wild-type animals."
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"However, we found that bec-1 and beclin1 RNAi still reduced the number of mitotic germ cells in the gld-2 (q497) gld-1 (q1485); glp-1 (q175) triple mutants to a similar extent as in wild-type animals (XREF_SUPPLEMENTARY)."
KCNH3 activates GCG.
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KCNH3 activates GCG. 2 / 2
| 2
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"In contrast, loss of BEC-1 function further decreased germ cell proliferation in the glp-1 (e2141lf) loss of function allele (XREF_SUPPLEMENTARY), which is characterized by a reduction in germline progenitors, and a severe Glp (Germline abnormal proliferation) phenotype, where germ cells do not proliferate and differentiate prematurely [XREF_BIBR]."
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"We found that RNAi inhibition of unc-51, bec-1, vps-34, lgg-1, and atg-18 each significantly reduced the mean lifespan of glp-1 (e2141) animals (XREF_FIG and XREF_SUPPLEMENTARY), and we observed similar results with an additional germline deficient mutant, mes-1 (bn7) [XREF_BIBR] (XREF_SUPPLEMENTARY)."
PIK3C3 affects KCNH3
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| 2 2
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"To exclude the possibility that 5-FU-induced autophagy could be an artefact of the transgenic reporter system used, we monitored the expression of the endogenous VPS-34 protein (a homologue of human class III PI3K) that interacts with BEC-1 ( xref )."
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"Loss of sorf-1 or sorf-2 did not affect the BEC-1 and VPS-34 interaction, because similar levels of Flag-VPS-34 were coprecipitated with BEC-1 in N2, sorf-1 (tm3855), and sorf-2 (tm5210) animals (XREF_FIG)."
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"Loss-of-function of components of the autophagy pathway, including the VPS-34 and BEC-1 complex, causes accumulation of PGL-1 and PGL-3 into aggregates in somatic cells (termed PGL granules)."
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"In C. elegans , BEC-1 interacts with the class III PI3 kinase VPS-34 (LET-512) [ xref ], an essential protein required for autophagy, membrane trafficking and endocytosis."
KCNH3 affects cell death
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KCNH3 inhibits cell death.
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| 2
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"Loss of function in the key autophagy factor beclin and bec -1 rescues the organismal death of gpb-2 mutants, confirming that elevated autophagy was the cause of death."
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"37 Thus, a reasonable hypothesis for the mechanism of the hypoxia hypersensitive phenotype of bec-1 (RNAi) animals is that knockdown of BEC-1 activity increases apoptotic cell death and thereby sensitize animals to hypoxic injury."
KCNH3 activates cell death.
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"Thus, our results are consistent with bec-1 inactivation enhancing apoptotic death following hypoxia, perhaps through a direct disinhibition of the canonical apoptosis pathway."
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"72 In C. elegans, BEC-1 was shown to interact with the Bcl-2 homolog CED-9, and inactivation of bec-1 produced ectopic apoptotic cell death."
KCNH3 affects PIK3C3
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| 2 2
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"To exclude the possibility that 5-FU-induced autophagy could be an artefact of the transgenic reporter system used, we monitored the expression of the endogenous VPS-34 protein (a homologue of human class III PI3K) that interacts with BEC-1 ( xref )."
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"Loss of sorf-1 or sorf-2 did not affect the BEC-1 and VPS-34 interaction, because similar levels of Flag-VPS-34 were coprecipitated with BEC-1 in N2, sorf-1 (tm3855), and sorf-2 (tm5210) animals (XREF_FIG)."
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"Loss-of-function of components of the autophagy pathway, including the VPS-34 and BEC-1 complex, causes accumulation of PGL-1 and PGL-3 into aggregates in somatic cells (termed PGL granules)."
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"In C. elegans , BEC-1 interacts with the class III PI3 kinase VPS-34 (LET-512) [ xref ], an essential protein required for autophagy, membrane trafficking and endocytosis."
BCL2 affects KCNH3
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BCL2 inhibits KCNH3.
| 1 1
BCL2 inhibits KCNH3. 2 / 2
| 1 1
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"The autophagic activity of Bec-1 relies on its disassociation from Bcl-2 that in turn only inhibits Bec-1 when it is localized to the ER."
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"The autophagic activity of Bec-1 relies on its disassociation from Bcl-2 that in turn only inhibits Bec-1 when it is localized to the ER."
BCL2 binds KCNH3.
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| 1 1
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"Additionally, similar to mammals, BEC-1, a component of the class III Phosphatidylinositol 3-Kinase (PI3K) complex ( xref ), interacts with the anti-apoptotic ortholog of Bcl-2, CED-9, suggesting cross-talk between autophagy and apoptosis ( xref ; xref )."
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"Furthermore, BEC-1 forms a complex with the antiapoptotic protein CED-9 and Bcl-2, and its depletion triggers CED-3 and Caspase-dependent PCD."
KCNH3 affects FOXG1
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KCNH3 increases the amount of FOXG1.
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KCNH3 increases the amount of FOXG1. 2 / 2
| 2
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"In contrast to its repressive function in Cdkn1a transcription, FOXG1 activated Kcnh3 transcription."
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"FOXG1 activates Kcnh3 transcription."
KCNH3 activates FOXG1.
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KCNH3 activates FOXG1. 1 / 1
| 1
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"We concluded that Kcnh3 is a direct target of FOXG1 and that its expression is mainly confined to mature neurons, the generation of which is impaired in Foxg1 deficient mice."
FOXO affects KCNH3
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FOXO activates KCNH3. 3 / 3
| 3
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"Whether bec-1 and lgg-1 are directly activated by FOXO and DAF -16 in worms is unknown, but both genes are transcriptionally activated by FOXO in mammals."
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"To further corroborate the notion that bec-1 and beclin1 acts independently of daf-16 and FOXO, we analyzed a daf-16 (mgDf47); bec-1 (ok691) double mutant, and found that complete loss of daf-16 and FOXO also failed to suppress the bec-1 and beclin1 mutant phenotype (XREF_FIG)."
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"To further corroborate the notion that bec-1 and beclin1 acts independently of daf-16 and FOXO, we analyzed a daf-16 (mgDf47); bec-1 (ok691) double mutant and found that complete loss of daf-16 and FOXO also failed to suppress the bec-1 and beclin1 mutant phenotype."
Daf-16 affects KCNH3
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Daf-16 activates KCNH3. 2 / 2
| 2
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"To further corroborate the notion that bec-1 and beclin1 acts independently of daf-16 and FOXO, we analyzed a daf-16 (mgDf47); bec-1 (ok691) double mutant, and found that complete loss of daf-16 and FOXO also failed to suppress the bec-1 and beclin1 mutant phenotype (XREF_FIG)."
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"To further corroborate the notion that bec-1 and beclin1 acts independently of daf-16 and FOXO, we analyzed a daf-16 (mgDf47); bec-1 (ok691) double mutant and found that complete loss of daf-16 and FOXO also failed to suppress the bec-1 and beclin1 mutant phenotype."
Ar202gf affects KCNH3
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Ar202gf inhibits KCNH3. 2 / 2
| 2
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"Interestingly, the glp-1 (ar202gf) allele suppressed the mitotic germline proliferation defect of mutations in bec-1 and Beclin1, atg-16.2/ATG16L, or atg-18/WIPI1/2 to wild-type levels, but not to the level of glp-1 (ar202gf) alone (XREF_SUPPLEMENTARY), suggesting that autophagy has a GLP-1 independent activity in promoting germline stem cell proliferation."
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"Interestingly, the glp-1 (ar202gf) allele suppressed the mitotic germline proliferation defect of mutations in bec-1 and Beclin1, atg-16.2/ATG16L, or atg-18/WIPI1/2 to wild-type levels, but not to the level of glp-1 (ar202gf) alone, suggesting that autophagy has a GLP-1-independent activity in promoting germline stem cell proliferation."
RNAi affects KCNH3
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RNAi inhibits KCNH3. 2 / 2
| 2
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"In double mutants of rab-7 with sorf-1 or sorf-2, RNAi depletion of vps-34, bec-1, or Y34B4a.2, which encodes the C. elegans homolog of UVRAG, strongly suppressed the enlargement of early endosomes in hypodermal cells (XREF_FIG)."
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"Interestingly, we found that RNAi mediated inhibition of bec-1, lgg-1, vps-34, or the putative autophagy inducer pha-4 all significantly reduced the lifespan of LIPL-4 overexpressing animals, while having negligible effects on non transgenic siblings (XREF_FIG, and XREF_SUPPLEMENTARY)."
PTEN affects KCNH3
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PTEN inhibits KCNH3. 2 / 2
| 2
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"Instead, BEC-1 and Beclin acts in a DAF-2 and IIR-dependent non canonical pathway through the transcriptional regulator SKN-1 and Nrf (rather than DAF-16 and FOXO), and is negatively regulated by DAF-18 and PTEN (XREF_FIG)."
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"Instead, BEC-1 and Beclin1 acts in a DAF-2 and IIR-dependent, non canonical pathway through the transcriptional regulator SKN-1 and Nrf (rather than DAF-16 and FOXO) and is negatively regulated by DAF-18 and PTEN."
KCNH3 affects bec-1 mutants
| 2
KCNH3 activates bec-1 mutants. 2 / 2
| 2
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"In contrast, expression of bec-1 from an intestinal promoter [P glo-1 : : BEC-1] did not rescue the proliferation defect of bec-1 mutants."
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"In contrast, expression of bec-1 from an intestinal promoter [Pglo-1 : : BEC-1] did not rescue the proliferation defect of bec-1 mutants (XREF_FIG)."
KCNH3 affects BCL2
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| 1 1
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"Additionally, similar to mammals, BEC-1, a component of the class III Phosphatidylinositol 3-Kinase (PI3K) complex ( xref ), interacts with the anti-apoptotic ortholog of Bcl-2, CED-9, suggesting cross-talk between autophagy and apoptosis ( xref ; xref )."
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"Furthermore, BEC-1 forms a complex with the antiapoptotic protein CED-9 and Bcl-2, and its depletion triggers CED-3 and Caspase-dependent PCD."
GCG affects KCNH3
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GCG inhibits KCNH3. 2 / 2
| 2
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"Interestingly, the glp-1 (ar202gf) allele suppressed the mitotic germline proliferation defect of mutations in bec-1 and Beclin1, atg-16.2/ATG16L, or atg-18/WIPI1/2 to wild-type levels, but not to the level of glp-1 (ar202gf) alone (XREF_SUPPLEMENTARY), suggesting that autophagy has a GLP-1 independent activity in promoting germline stem cell proliferation."
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"Interestingly, the glp-1 (ar202gf) allele suppressed the mitotic germline proliferation defect of mutations in bec-1 and Beclin1, atg-16.2/ATG16L, or atg-18/WIPI1/2 to wild-type levels, but not to the level of glp-1 (ar202gf) alone, suggesting that autophagy has a GLP-1-independent activity in promoting germline stem cell proliferation."
DAF-18 affects KCNH3
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DAF-18 inhibits KCNH3. 2 / 2
| 2
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"Instead, BEC-1 and Beclin acts in a DAF-2 and IIR-dependent non canonical pathway through the transcriptional regulator SKN-1 and Nrf (rather than DAF-16 and FOXO), and is negatively regulated by DAF-18 and PTEN (XREF_FIG)."
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"Instead, BEC-1 and Beclin1 acts in a DAF-2 and IIR-dependent, non canonical pathway through the transcriptional regulator SKN-1 and Nrf (rather than DAF-16 and FOXO) and is negatively regulated by DAF-18 and PTEN."
CHN1 affects KCNH3
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Modified CHN1 inhibits KCNH3. 1 / 1
| 1
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"In contrast, loss of ubc-13 or chn-1 caused a significant reduction in the protein levels of VPS-34 but not BEC-1."
CHN1 inhibits KCNH3. 1 / 1
| 1
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"We found that loss of chn-1 enhanced the cell corpse phenotype of piki-1 (ok2346) but not vps-34 (qx467) or bec-1 (ok700) mutants (XREF_FIG and Fig."
SORF2 affects KCNH3
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SORF2 inhibits KCNH3. 1 / 1
| 1
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"The membrane-to-cytoplasm ratio of YFP : : BEC-1 intensity was higher in sorf-1 and sorf-2 mutants than in wild type (XREF_FIG), suggesting that SORF-1 and SORF-2 may prevent BEC-1 from accessing early endosomes."
SORF1 affects KCNH3
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SORF1 inhibits KCNH3. 1 / 1
| 1
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"The membrane-to-cytoplasm ratio of YFP : : BEC-1 intensity was higher in sorf-1 and sorf-2 mutants than in wild type (XREF_FIG), suggesting that SORF-1 and SORF-2 may prevent BEC-1 from accessing early endosomes."
Pha-4 affects KCNH3
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Modified pha-4 increases the amount of KCNH3. 1 / 1
| 1
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"Notably, we found that overexpression of PHA-4 significantly induced unc-51 but not lgg-1 and bec-1 levels (XREF_SUPPLEMENTARY), suggesting that PHA-4 overexpression is sufficient to recapitulate some, but not all of the PHA-4 mediated effects observed in glp-1 animals."
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Transcriptionally active hsa-miR-335-5p decreases the amount of KCNH3. 1 / 1
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biopax:mirtarbase
No evidence text available
Env affects KCNH3
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"Thus, gp120 and BEC1 interaction may be involved in HIV-1 life cycle and/or pathogenesis."
Dihydrogen affects KCNH3
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"We show here that Kv10.2, Kv12.2, and Kv12.3 are similarly inhibited by external protons, suggesting that high sensitivity to physiological pH changes is a general property of EAG superfamily channels."
UBE2N affects KCNH3
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Modified UBE2N inhibits KCNH3. 1 / 1
| 1
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"In contrast, loss of ubc-13 or chn-1 caused a significant reduction in the protein levels of VPS-34 but not BEC-1."
PI3K affects KCNH3
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"One recent approach that investigated the interaction between the autophagy gene Bec-1 and Phosphoinositide 3-kinase revealed a candidate peptide (Tat-becline 1) for inducing anti-bacterial autophagy."
KCNH3 affects rict-1 mutants
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KCNH3 activates rict-1 mutants. 1 / 1
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"Surprisingly, RNAi of autophagy components bec-1 (C. elegans Beclin1 homolog) and lgg-1 restored normal lifespan in short lived sgk-1 and rict-1 mutants (XREF_FIG - XREF_FIG)."
KCNH3 affects paraquat
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"RNAi of bec-1 or ant-1.1 also attenuates paraquat toxicity in rict-1 and sgk-1 mutants and vdac-1 overexpressers, and even moderately in wild type animals (XREF_SUPPLEMENTARY - XREF_SUPPLEMENTARY)."
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"Nevertheless, we can conclude that BEC-1 activity inhibits necrotic cell death after a hypoxic insult."
KCNH3 affects gpb-2 mutants
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KCNH3 inhibits gpb-2 mutants. 1 / 1
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"Loss of function in the key autophagy factor beclin and bec -1 rescues the organismal death of gpb-2 mutants, confirming that elevated autophagy was the cause of death."
KCNH3 affects env
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"Thus, gp120 and BEC1 interaction may be involved in HIV-1 life cycle and/or pathogenesis."
KCNH3 affects daf-2 mutants
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KCNH3 activates daf-2 mutants. 1 / 1
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"Together, these findings suggest that bec-1 and daf-16 act in parallel pathways to increase the lifespan of daf-2 mutants."
KCNH3 affects daf-2
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KCNH3 inhibits daf-2. 1 / 1
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"In C. elegans , downregulation of the autophagy gene Bec1 inhibited the longevity phenotype of the Daf-2 insulin receptor mutant [ xref ], indicating that the extension of lifespan due to alterations in insulin signaling may occur, at least in part, via autophagy."
KCNH3 affects TOR
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KCNH3 activates TOR. 1 / 1
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"However, recent studies in C. elegans suggest a direct role for autophagy in modulating longevity, as inactivation of autophagy genes (bec-1, unc-51, atg-18) specifically prevents inhibition of TOR activity from extending lifespan [XREF_BIBR, XREF_BIBR]."
KCNH3 affects SLC6A4
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KCNH3 activates SLC6A4. 1 / 1
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"Knockdown of bec-1, atg-7 and atg-18 caused the accumulation of HTT protein aggregates in transgenic worms expressing HTT-Q150 in muscles and sensory neurons."
KCNH3 affects SGK1
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KCNH3 activates SGK1. 1 / 1
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"Surprisingly, RNAi of autophagy components bec-1 (C. elegans Beclin1 homolog) and lgg-1 restored normal lifespan in short lived sgk-1 and rict-1 mutants (XREF_FIG - XREF_FIG)."
KCNH3 affects Proteasome
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"These results indicate that BEC-1 negatively regulates the proteasome activity XREF_BIBR."
KCNH3 affects PI3K
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"One recent approach that investigated the interaction between the autophagy gene Bec-1 and Phosphoinositide 3-kinase revealed a candidate peptide (Tat-becline 1) for inducing anti-bacterial autophagy."
KCNH3 affects INSR
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KCNH3 inhibits mutated INSR. 1 / 1
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"In C. elegans, downregulation of the autophagy gene Bec1 inhibited the longevity phenotype of the Daf-2 insulin receptor mutant [XREF_BIBR], indicating that the extension of lifespan due to alterations in insulin signaling may occur, at least in part, via autophagy."
KCNH3 affects HSF1
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KCNH3 decreases the amount of HSF1. 1 / 1
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"Moreover, RNAi of unc-51 and ATG1 and bec-1 and ATG6 abolished the protective effect of HSF-1 overexpression on aggregation formation, similar to our observations with hormetic heat shock (XREF_FIG and XREF_SUPPLEMENTARY)."
KCNH3 affects EPG-8
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KCNH3 binds EPG-8. 1 / 1
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"The epg-8 (ok2561) allele deletes both coiled coil domains necessary for EPG-8 binding to BEC-1, and epg-8 mutant embryos fail to accumulate LGG-1-positive autophagosomes."
KCNH3 affects BECN1
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KCNH3 bound to ced-9 inhibits BECN1. 1 / 1
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"The interaction between Beclin-1 and pro survival Bcl-2, used to inhibit autophagy, is conserved in the nematode model, with BEC-1 and CED-9 protein interactions disrupting the formation of the Beclin-1 initiation complex."
FOXO3 affects KCNH3
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FOXO3 increases the amount of KCNH3. 1 / 1
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"We concluded that Kcnh3 expression is increased by FOXG1 and FOXO3, but is independent of FOXO1 and TGFbeta signaling."
EPG-8 affects KCNH3
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KCNH3 binds EPG-8. 1 / 1
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"The epg-8 (ok2561) allele deletes both coiled coil domains necessary for EPG-8 binding to BEC-1, and epg-8 mutant embryos fail to accumulate LGG-1-positive autophagosomes."
CD55 affects KCNH3
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CD55 activates KCNH3. 1 / 1
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"Whether bec-1 and lgg-1 are directly activated by FOXO and DAF -16 in worms is unknown, but both genes are transcriptionally activated by FOXO in mammals."
BCL2L1 affects KCNH3
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BCL2L1 inhibits KCNH3. 1 / 1
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"Bcl-XL has also been implicated to reduce the pro autophagic activity of Bec-1 (Amelio et al., 2011; Maiuri et al., 2007; Pattingre et al., 2005)."