Datasheet

生物学的記述

Specificity	MLX Antibody [N17K22] detects endogenous levels of total MLX protein.
Background	MLX, a basic helix-loop-helix leucine zipper transcription factor in the Myc/Max/Mad superfamily, heterodimerizes obligatorily with tissue-specific partners MLXIP (MondoA) or MLXIPL (ChREBP) to sense glucose metabolites and regulate metabolic gene expression. Both complexes feature bHLHZip domains for E-box (CACGTG) DNA binding and N-terminal activation domains responsive to glucose-6-phosphate via hexokinase-catalyzed phosphorylation, with cytoplasmic-mitochondrial retention in low glucose shifting to nuclear accumulation upon metabolite elevation. MLX/MLXIP heterodimers translocate rapidly to the nucleus following 2-deoxyglucose exposure, binding ChoRE promoters of thioredoxin-interacting protein (TXNIP), ARRDC4, and glycolytic enzymes like HK2, PFKFB3, LDH-A to drive >75% of glucose-induced transcription, while promoting histone H4 acetylation for open chromatin. MLX/MLXIPL similarly activates lipogenic targets in the liver, with MLX phosphorylation stabilizing heterotetramers on DNA for sustained activity. Glucose sensing integrates hexokinase activity, as inhibitors like 3-bromopyruvate block nuclear import, and MondoA mutations disrupting MLX dimerization abolish response. MLX orchestrates glucose homeostasis by inducing glycolysis/lipogenesis genes and repressing uptake via TXNIP, balancing nutrient flux in muscle, liver, and proliferating cells. MLX-null impairs myokine secretion, including IGF2 for myoblast fusion/Akt activation, blunts muscle regeneration, and disrupts sugar tolerance/lipid balance. Dysregulation contributes to diabetes through failed TXNIP induction and cancer via Myc cooperation, reprogramming metabolism.

Specificity

MLX Antibody [N17K22] detects endogenous levels of total MLX protein.

Background

MLX, a basic helix-loop-helix leucine zipper transcription factor in the Myc/Max/Mad superfamily, heterodimerizes obligatorily with tissue-specific partners MLXIP (MondoA) or MLXIPL (ChREBP) to sense glucose metabolites and regulate metabolic gene expression. Both complexes feature bHLHZip domains for E-box (CACGTG) DNA binding and N-terminal activation domains responsive to glucose-6-phosphate via hexokinase-catalyzed phosphorylation, with cytoplasmic-mitochondrial retention in low glucose shifting to nuclear accumulation upon metabolite elevation. MLX/MLXIP heterodimers translocate rapidly to the nucleus following 2-deoxyglucose exposure, binding ChoRE promoters of thioredoxin-interacting protein (TXNIP), ARRDC4, and glycolytic enzymes like HK2, PFKFB3, LDH-A to drive >75% of glucose-induced transcription, while promoting histone H4 acetylation for open chromatin. MLX/MLXIPL similarly activates lipogenic targets in the liver, with MLX phosphorylation stabilizing heterotetramers on DNA for sustained activity. Glucose sensing integrates hexokinase activity, as inhibitors like 3-bromopyruvate block nuclear import, and MondoA mutations disrupting MLX dimerization abolish response. MLX orchestrates glucose homeostasis by inducing glycolysis/lipogenesis genes and repressing uptake via TXNIP, balancing nutrient flux in muscle, liver, and proliferating cells. MLX-null impairs myokine secretion, including IGF2 for myoblast fusion/Akt activation, blunts muscle regeneration, and disrupts sugar tolerance/lipid balance. Dysregulation contributes to diabetes through failed TXNIP induction and cancer via Myc cooperation, reprogramming metabolism.

使用情報

Application

WB, IP, ChIP

Dilution

WB	IP	CHIP
1:1000	1:100	1:100

Reactivity

Human, Mouse, Rat, Monkey

Source

Rabbit Monoclonal Antibody

MW

30 kDa

Storage Buffer

PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage
(from the date of receipt)

-20°C (avoid freeze-thaw cycles), 2 years

プロトコール

References

https://pubmed.ncbi.nlm.nih.gov/26584623/
https://pubmed.ncbi.nlm.nih.gov/18458340/

MLX Antibody [N17K22]

生物学的記述

使用情報

References

Application Data