EC Number   |
General Information |
Reference |
|---|
    1.3.1.70 | evolution |
the enzyme belongs to the sterol reductase family |
-, 745882 |
| 1.3.1.70 | malfunction |
Arabidopsis thaliana weak mutant allele fk-J3158, impaired in the FACKEL (FK) gene, which encodes the C-14 reductase, has a long life cycle and delayed flowering time in different photoperiods. Enzyme overexpression lines display an earlier flowering phenotype than that of the wild-type, flowering time of fk-J3158 flc double mutant is significantly earlier than that of fk-J3158 under the long-day conditions. These processes might be independent of the downstream brassinosteroid pathway and the autonomous pathway. The fk-J3158 plants are more sensitive than wild-type in reducing the bolting days and total leaf number under gibberellic acid treatment. Enzyme mutation leads to an absence of endogenous gibberellic acids in fk-J3158 and FK gene expression also affected under gibberellic acid and paclobutrazol treatment. The delayed flowering time of fk-J3158 is rescued by a 3-week vernalization treatment, and the expression of flowering locus C C (FLC) is accordingly downregulated in fk-J3158. Flowering time of fk-J3158 flc double mutant is significantly earlier than that of fk-J3158 under the long-day conditions. Phenotypes, detailed overview |
746161 |
| 1.3.1.70 | malfunction |
FgERG24A and FgERG24B are deleted in Fusarium graminearum. Compared to the wild-type strain HN9-1, FgERG24A and FgERG24B deletion mutants do not show recognizable phenotypic changes in mycelial growth on potato dextrose agar or in virulence on wheat heads. FgERG24B deletion mutants exhibit significantly increased sensitivity to amine fungicides, including tridemorph, fenpropidin and spiroxamine. FgERG24A deletion mutants do not show changed sensitivity to any amine tested. The resistance of the FgERG24B deletion mutant to amines is restored by genetic complementation of the mutant with wild-type FgERG24B |
725903 |
| 1.3.1.70 | malfunction |
inactivation of both homologs of Erg24 results in decreased hyphal growth and virulence, leads to the disruption of ion homeostasis and affects ergosterol biosynthesis. Loss of one homolog of Erg24 impairs hyphal growth, conidiation, and virulence but has no effect on ergosterol biosynthesis |
-, 763997 |
| 1.3.1.70 | malfunction |
Tm7sf2 deficiency during liver regeneration alters lipid metabolism and generates a stress condition, which, in turn, transiently unbalances hepatocytes cell cycle progression. Tm7sf2 knockout mice show no alteration in cholesterol content, but accumulation and delayed catabolism of hepatic triglycerides is observed, resulting in persistent steatosis at all times post hepatectomy. Delayed cell cycle progression to the G1/S phase is observed in Tm7sf2 knockout mice, resulting in reduced cell division at the time points examined associated to abnormal endoplasmic reticulum stress response, leading to alteration in p53 content and, consequently, induction of p21 expression in Tm7sf2 knockout mice. Tm7sf2 knockout mice exhibit a high-degree of transient hepatic steatosis during liver regeneration after partial hepatectomy. Hepatocytes from Tm7sf2 KO mice have a defective progression through the G1/S phase, associated to delayed and/or reduced expression of central regulators of the cell cycle such as cyclin D1, cyclin A, cyclin E1 and CDK4 |
744648 |
| 1.3.1.70 | metabolism |
an inverse upregulation of lanosterol 14alpha-demethylase, CYP51, and downregulation of 14-SR expression under luteinizing hormone/follicle stimulating hormone stimulation functions as the machinery for FF-MAS accumulation in preovulatory follicles prior to ovulation in the rabbit, overview |
713446 |
| 1.3.1.70 | metabolism |
the enzyme is involved in the cholesterol biosynthesis pathway |
-, 745882 |
| 1.3.1.70 | more |
the enzyme contains ten transmembrane segments (TM1-10). Its catalytic domain comprises the carboxy-terminal half (containing TM6-10) and envelops two interconnected pockets, one of which faces the cytoplasm and houses NADPH, while the other one is accessible from the lipid bilayer. The reducing end of NADPH meets the sterol substrate at the juncture of the two pockets |
-, 745882 |
| 1.3.1.70 | more |
TM7SF2 gene expression is controlled by cell sterol levels through the SREBP-2, motifs of TM7SF2 promoter responsible for activation by SREBP-2 are the SRE motif, and both the inverted CCAAT-box and GC-box2, which are essential for full promoter activation by SREBP-2, overview. Binding of SREBP-2 to SRE produces approximately 26fold promoter activation, whereas mutation of the SRE motif causes a dramatic decrease of transactivation by SREBP-2 |
711302 |
| 1.3.1.70 | physiological function |
both erg24A and erg24B homologs in combination, but not individuall, are essential for the viability of Aspergillus fumigatus. The enzyme plays a critical role in ergosterol biosynthesis and ion homeostasis |
-, 763997 |
