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1                                              SREBP1 and SREBP2 share approximately 47% sequence ident
2                                              SREBP1 cleavage is normally inhibited by increased stero
3                                              SREBP1 inhibition augmented the efficacy of immune check
4                                              SREBP1 levels were higher after PTEN knockdown and may a
5                                              SREBP1 predominantly binds to the transcription start si
6                                              SREBP1's stability is determined by a degradation signal
7 sterol regulatory element-binding protein 1 (SREBP1) degradation in conferring the response of EGFR m
8 sterol regulatory element binding protein 1 (SREBP1) mediates the induction of steatosis by upregulat
9 , sterol response element binding protein 1 (SREBP1) was identified as a novel lamin A interactor.
10 e sterol response element-binding protein 1 (SREBP1) was implicated in the nutrient control of lipoge
11 Sterol regulatory element-binding protein 1 (SREBP1), when presented in its mature form (mSREBP1), en
12 sterol regulatory element-binding protein 1 (SREBP1), which promotes the transcription of lipogenes i
13 sterol regulatory element-binding protein 1 (SREBP1)-directed transcription of its direct targets inc
14 sterol regulatory element-binding protein 1 (SREBP1)-mediated fatty acid synthesis in immunosuppressi
15 sterol regulatory element-binding protein 1 (SREBP1)-mediated pathway through which miR-148a regulate
16 e sterol response element binding protein 1 (SREBP1).
17 sterol regulatory element-binding protein 1 (SREBP1).
18 sterol regulatory element-binding protein 1 (SREBP1).
19 d sterol response element binding protein 1 (SREBP1).
20 r sterol response element-binding protein-1 (SREBP1) and Spot 14 as biohydrogenation intermediate res
21 sterol regulatory element binding protein-1 (SREBP1) appear to be crucial for the response of the UCP
22 sterol regulatory element-binding protein-1 (SREBP1) remodels such metabolic cascade.
23  sterol regulatory element-binding protein 1(SREBP1/SREBF1), in a PI3K-mTORC1-dependent fashion.
24  droplet accumulation possibly via the ABCA1-SREBP1/2 pathway.
25  deficient of SUMO-binding fails to activate SREBP1/2 and lipogenesis due to impaired SREBP binding a
26 genes (Insig1/2(Delta/Delta) mice) activated SREBP1, causing marked accumulation of lipids that consi
27                               VEGF activated SREBP1 and SREBP2 in ECs, as demonstrated by the increas
28 l tissues was inversely correlated to active SREBP1.
29 rs including PPARgamma, the C/EBPs, and ADD1/SREBP1.
30 lement consensus and specifically binds ADD1/SREBP1.
31         The stimulation of PPARgamma by ADD1/SREBP1 does not require coexpression in the same cells;
32 th leptin and FAS are transactivated by ADD1/SREBP1.
33 supernatants from cultures that express ADD1/SREBP1 augment the transcriptional activity of PPARgamma
34 onstrate directly that cells expressing ADD1/SREBP1 produce and secrete lipid molecule(s) that bind d
35  that most if not all of this action of ADD1/SREBP1 is through an E-box motif at -64 to -59, containe
36     We show here that the expression of ADD1/SREBP1 specifically increases the activity of PPARgamma
37       A mutation in the basic domain of ADD1/SREBP1 that allows E-box binding but destroys sterol reg
38                       This elevation of ADD1/SREBP1, leptin, and FAS that is induced by feeding in vi
39               These data establish that ADD1/SREBP1 can control the production of endogenous ligand(s
40             These results indicate that ADD1/SREBP1 is a key transcription factor linking changes in
41 red with the interaction between lamin A and SREBP1.
42 phosphorylation of the AR, ACK1, ATPF1A, and SREBP1 at Y267, Y284, Y243/Y246, and Y673/Y951, respecti
43 selective ER stress markers GRP78, CHOP, and SREBP1 was increased equivalently in both types of mice.
44 s pathway, such as PPARgamma, C/EBPalpha and SREBP1.
45 known partners, including actin, emerin, and SREBP1, but how these interactions are regulated is unkn
46 broblasts by significantly reducing LDLr and SREBP1 gene expression.
47 ; however, the connection between mTORC2 and SREBP1 has not been clearly established and hence is the
48 d a novel connection between osimertinib and SREBP1 degradation and its impact on the response of EGF
49 he insulin signalling genes IRS2, PIK3CB and SREBP1-c in skeletal muscle and perirenal fat, favouring
50 sis suggested that HFD/WD induces SPTBN1 and SREBP1 cleavage by CASPASE-3 and that the cleaved produc
51 rexpression, and DAXX mutants unable to bind SREBP1/2 have weakened activity in promoting lipogenesis
52 aster regulator of cholesterol biosynthesis, SREBP1.
53 d found reduced adipogenesis, accompanied by SREBP1 downregulation.
54           Consistent with our in vitro data, SREBP1 was detected in newly developed microvasculatures
55 s cell-membrane permeable, disrupts the DAXX-SREBP1/2 interactions, and inhibits lipogenesis and tumo
56 ranscription factors (PPARgamma, C/EBPalpha, SREBP1) of the adipogenesis pathway.
57 osis, whereas enforced expression of ectopic SREBP1 in sensitive EGFR-mutant NSCLC cells compromised
58                            The gene encoding SREBP1 (SREBF1) has been cloned and characterized.
59 solated human adipocytes to insulin enhanced SREBP1 gene expression and promoted its proteolytic clea
60 ding of the adipoctye differentiation factor SREBP1 to lamin A.
61 eracts with a lipogenic transcription factor SREBP1 at active promoters, thereby bridging the newly t
62 ocused on the lipogenic transcription factor SREBP1.
63 lement-binding (SREBP) transcription factors SREBP1 and 2, whose activation and mRNA expression are s
64 ectly through SIRT1, it is also required for SREBP1 binding to the FAS promoter.
65 f evidence suggest that LSD1 is required for SREBP1-dependent activation of the FAS promoter in mamma
66 poorly or not activating the lipogenic genes SREBP1 and SCD1 or FASN, respectively.
67 andial rise in triglyceride synthesis genes (SREBP1-c, FAS, SCD-1).
68 pression and proteolytic maturation of human SREBP1 are positively modulated by insulin.
69 l clones provided an opportunity to identify SREBP1-regulated genes that may influence the assembly a
70          Altogether, these results implicate SREBP1 and DNFA enzymes as enticing therapeutic targets
71  not the degradation signal, is conserved in SREBP1.
72                       Oxysterols inactivated SREBP1 in wild type macrophages but not in LDLR(-/-) cel
73 transcription factors and enzymes, including SREBP1 and PNPLA3, as demonstrated by microarray analysi
74 yperinsulinemia also significantly increased SREBP1 gene expression in human skeletal muscle.
75              We observed that KRAS increases SREBP1 expression and genetic knockdown of SREBP1 signif
76 chanistically, statins and NSDHL loss induce SREBP1 activation, which promotes the expression of Tgfb
77 d SMAD3 and limits lipogenesis by inhibiting SREBP1 and SREBP2 activity.
78 tive mechanism in WAT, which involves Insig1/SREBP1 and preserves the degree of lipid unsaturation un
79 ulatory feedback set point control of Insig1/SREBP1 represent an adaptive response that preserves WAT
80 p between (i) the cellular content of mature SREBP1 and 7alpha-hydroxylase protein, (ii) the relative
81     The increased cellular content of mature SREBP1 and increased secretion of apoB100 were concomita
82 l clones expressed varying amounts of mature SREBP1 protein.
83 terol, suggesting that the content of mature SREBP1, known to be decreased by 25-hydroxycholesterol,
84 inked through the cellular content of mature SREBP1.
85                                    Moreover, SREBP1 expression significantly increased the ability of
86        PUFA suppressed both the hepatic mRNA(SREBP1) through a PPARalpha-independent mechanism as wel
87  accumulated, glycogen stimulates the mTORC1/SREBP1 pathway to shift energy storage to lipogenesis.
88                          In skeletal muscle, SREBP1 expression was significantly reduced in type 2 di
89 tors of tumor growth controlled by E2F, MYC, SREBP1 and AKT3 pathways on the one hand, and differenti
90  correlated with the nuclear accumulation of SREBP1 in samples from patients with HCC, but also assoc
91            This process requires cleavage of SREBP1 by site-1-protease (S1P) and S2P and subsequent t
92 tely blocked the insulin-induced cleavage of SREBP1 protein.
93                              The cleavage of SREBP1 requires it to be in complex with SREBP cleavage
94 thesis, under the transcriptional control of SREBP1, is regulated by the rapamycin-sensitive mTOR sig
95 he N-terminal transcription factor domain of SREBP1, between residues 227 and 487.
96           Importantly, ectopic expression of SREBP1, the master regulator of lipogenic genes, in MCF1
97     Within the diabetic group, the extent of SREBP1 suppression was inversely related to metabolic co
98 acilitated degradation of the mature form of SREBP1 (mSREBP1) in a GSK3/FBXW7-dependent manner and re
99 tion of the transcriptionally active form of SREBP1.
100 d temperature induces circadian induction of SREBP1 that drives fuel synthesis in BAT and is necessar
101 th genetic and pharmacological inhibition of SREBP1 sensitized osimertinib-resistant cells and tumors
102                    In vitro investigation of SREBP1 variants demonstrated impaired S1P cleavage, whic
103 s SREBP1 expression and genetic knockdown of SREBP1 significantly inhibited the cell proliferation of
104 nd insulin-treated cells, the mRNA levels of SREBP1-c, SREBP2, fatty-acid synthase, acetyl-CoA carbox
105  a novel role, distinct from lipogenesis, of SREBP1 on mitochondrial function in mutant KRAS NSCLC.
106 ve response that promotes the maintenance of SREBP1 maturation and facilitates lipogenesis and availa
107       A role for mTORC1 in the regulation of SREBP1 activity has been suggested; however, the connect
108 y inhibition, whether by direct targeting of SREBP1 with antisense oligonucleotides, or through combi
109 s-promoting transcription factors PPARgamma, SREBP1, and CEBPalpha to prevent fat storage.
110           Here, we found that PRMT5 promoted SREBP1 SDM and the induction of cholesterol biosynthetic
111 d sterol regulatory element-binding protein (SREBP1 and SREBP2).
112  sterol regulatory element-binding proteins (SREBP1 and SREBP2) that are required for oncogene-induce
113 apparatus, the activation of SREBP proteins (SREBP1 or SREBP2) and the transcription of downstream li
114 we show that LSD1 plays a role in regulating SREBP1-mediated gene expression.
115 to activation of master lipogenic regulators SREBP1/2.
116 rmation of master lipid-metabolic regulators SREBP1/2, concentrating transcriptional co-activators to
117                                 As a result, SREBP1 variants exhibited significantly lower transcript
118    In this report, we have assessed the role SREBP1 plays in the PUFA control of three hepatic genes,
119 s that PPDPF negatively regulates mTORC1-S6K-SREBP1 signaling.
120  in primary hepatocytes, CA-FoxO1 suppressed SREBP1-c expression and inhibited basal and insulin-indu
121 complex 1 (mTORC1) and its downstream target SREBP1.
122 lidating the strategy via directly targeting SREBP1 for overcoming osimertinib acquired resistance.
123 ossibly other EGFR inhibitors, via targeting SREBP1.
124 sterol homeostasis (where it has been termed SREBP1).
125                                 We find that SREBP1 and 2 promote proliferation downstream of mTORC1,
126                                 We find that SREBP1-regulated DNFA represents a survival trait in mel
127  using short hairpin RNA (shRNA) showed that SREBP1 cleavage and the induction of lipogenic genes and
128 alpha(i2) promoter activity, suggesting that SREBP1 may play a role in the regulation of Galpha(i2) e
129 on correlates with increased cleavage of the SREBP1 precursors to form the mature active transcriptio
130 Elevated DNFA gene expression depends on the SREBP1 transcription factor in multiple melanoma cell li
131                      They also show that the SREBP1-mediated induction of hepatic steatosis in ob/ob
132                             We find that the SREBP1-SCD1 pathway is negatively impacted in the brains
133                    The binding of lamin A to SREBP1 was noticeably reduced by FPLD mutations.
134 ot significantly altered in cells subject to SREBP1 knockdown.
135                                     In turn, SREBP1 regulates the expression of key lipogenic enzymes
136 BXD8 increased membrane lipid saturation via SREBP1 and the lipid desaturase SCD1.
137 e, we show that miR-33b also cooperates with SREBP1 in regulating glucose metabolism by targeting pho
138         Mechanistically, DAXX interacts with SREBP1 and SREBP2 and activates SREBP-mediated transcrip

 
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