KLHL25 report

I. Expression across cell types

II. Expression across tissues

sc-RNAseq data

Insufficient scRNA-seq data for expression of KLHL25 at tissue level.

III. Associated gene sets

GO_0006511Biological processubiquitin-dependent protein catabolic process
GO_0016567Biological processprotein ubiquitination
GO_0032831Biological processpositive regulation of CD4-positive, CD25-positive, alpha-beta regulatory T cell differentiation
GO_0006446Biological processregulation of translational initiation
GO_0046321Biological processpositive regulation of fatty acid oxidation
GO_0045717Biological processnegative regulation of fatty acid biosynthetic process
GO_0005829Cellular componentcytosol
GO_0031463Cellular componentCul3-RING ubiquitin ligase complex
GO_0005737Cellular componentcytoplasm
GO_1990756Molecular functionubiquitin-like ligase-substrate adaptor activity

IV. Literature review

[source]
Gene nameKLHL25
Protein nameKelch-like protein 25 (Ectoderm-neural cortex protein 2) (ENC-2)
SynonymsENC2
DescriptionFUNCTION: Substrate-specific adapter of a BCR (BTB-CUL3-RBX1) E3 ubiquitin ligase complex involved in various processes, such as translation homeostasis and lipid synthesis . The BCR(KLHL25) ubiquitin ligase complex acts by mediating ubiquitination of hypophosphorylated EIF4EBP1 (4E-BP1): ubiquitination and subsequent degradation of hypophosphorylated EIF4EBP1 (4E-BP1) probably serves as a homeostatic mechanism to maintain translation and prevent eIF4E inhibition when eIF4E levels are low . The BCR(KLHL25) complex does not target EIF4EBP1 (4E-BP1) when it is hyperphosphorylated or associated with eIF4E . The BCR(KLHL25) complex also acts as a regulator of lipid synthesis by mediating ubiquitination and degradation of ACLY, thereby inhibiting lipid synthesis . BCR(KLHL25)-mediated degradation of ACLY promotes fatty acid oxidation and is required for differentiation of inducible regulatory T (iTreg) cells . .

AccessionsQ9H0H3
ENST00000337975.6