Product: HK2 Antibody
Catalog: BF0283
Description: Mouse monoclonal antibody to HK2
Application: WB IHC ELISA FACS
Reactivity: Human
Mol.Wt.: 102kDa; 102kD(Calculated).
Uniprot: P52789
RRID: AB_2833836

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Product Info

ELISA 1:10000, WB 1:500-1:2000, IHC 1:200-1:1000, FCM 1:200-1:400
*The optimal dilutions should be determined by the end user.

WB: For western blot detection of denatured protein samples. IHC: For immunohistochemical detection of paraffin sections (IHC-p) or frozen sections (IHC-f) of tissue samples. IF/ICC: For immunofluorescence detection of cell samples. ELISA(peptide): For ELISA detection of antigenic peptide.

Monoclonal [AFB1812]
HK2 antibody detects endogenous levels of total HK2.
Cite Format: Affinity Biosciences Cat# BF0283, RRID:AB_2833836.
Mouse IgG1 in phosphate buffered saline (without Mg2+ and Ca2+), pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol. Store at -20 °C. Stable for 12 months from date of receipt.


DKFZp686M1669; Hexokinase 2; Hexokinase 2 muscle; Hexokinase type II; Hexokinase-2; HK 2; HK II; HK2; HKII; HxK 2; HxK2; HXK2_HUMAN; Muscle form hexokinase;



Purified recombinant fragment of human HK2 expressed in E. Coli.

P52789 HXK2_HUMAN:

Predominant hexokinase isozyme expressed in insulin-responsive tissues such as skeletal muscle.

The hexokinases utilize Mg-ATP as a phosphoryl donor to catalyze the first step of intracellular glucose metabolism, the conversion of glucose to glucose- 6-phosphate. Four hexokinase isoenzymes have been identified, including hexokinase I (HXK I), hexokinase II (HXK II), hexokinase III (HXK III) and hexokinase IV (HXK IV, also designated glucokinase or GCK). Hexokinases I-III each contain an N-terminal cluster of hydrophobic amino acids. Glucokinase lacks the N-terminal hydrophobic cluster. The hydrophobic cluster is thought to be necessary for membrane binding. This is substantiated by the finding that glucokinase has lower affinity for glucose than do the other hexokinases .Hexokinase 2 is the predominant hexokinase isozyme expressed in insulin-responsive tissues such as skeletal muscle. Expression of this gene is insulin-responsive, and studies in rat suggest that it is involved in the increased rate of glycolysis seen in rapidly growing cancer cells.

PTMs - P52789 As Substrate

Site PTM Type Enzyme
M1 Acetylation
Y9 Phosphorylation
K41 Ubiquitination
K49 Ubiquitination
K62 Ubiquitination
K104 Ubiquitination
Y112 Phosphorylation
K147 Ubiquitination
T153 Phosphorylation
K173 Ubiquitination
K176 Ubiquitination
Y238 Phosphorylation
K290 Ubiquitination
Y301 Phosphorylation
K315 Ubiquitination
K323 Ubiquitination
T331 Phosphorylation
K337 Ubiquitination
S340 Phosphorylation
K346 Ubiquitination
S384 Phosphorylation
K401 Ubiquitination
S415 Phosphorylation
K418 Ubiquitination
S445 Phosphorylation
S449 Phosphorylation
K451 Ubiquitination
T457 Phosphorylation
Y461 Phosphorylation
K472 Ubiquitination
T473 Phosphorylation
K488 Ubiquitination
K492 Ubiquitination
K501 Ubiquitination
S506 Phosphorylation
K510 Ubiquitination
T514 Phosphorylation
K525 Ubiquitination
K624 Ubiquitination
K638 Ubiquitination
Y686 Phosphorylation
K738 Ubiquitination
K743 Ubiquitination
S746 Phosphorylation
Y749 Phosphorylation
T762 Phosphorylation
K763 Ubiquitination
K866 Ubiquitination
K873 Ubiquitination
K885 Ubiquitination
S897 Phosphorylation
K899 Ubiquitination
T905 Phosphorylation

Research Backgrounds


Catalyzes the phosphorylation of hexose, such as D-glucose and D-fructose, to hexose 6-phosphate (D-glucose 6-phosphate and D-fructose 6-phosphate, respectively). Mediates the initial step of glycolysis by catalyzing phosphorylation of D-glucose to D-glucose 6-phosphate. Plays a key role in maintaining the integrity of the outer mitochondrial membrane by preventing the release of apoptogenic molecules from the intermembrane space and subsequent apoptosis.

Subcellular Location:

Mitochondrion outer membrane>Peripheral membrane protein. Cytoplasm>Cytosol.
Note: The mitochondrial-binding peptide (MBP) region promotes association with the mitochondrial outer membrane (PubMed:29298880). The interaction with the mitochondrial outer membrane via the mitochondrial-binding peptide (MBP) region promotes higher stability of the protein (PubMed:29298880). Release from the mitochondrial outer membrane into the cytosol induces permeability transition pore (PTP) opening and apoptosis (PubMed:18350175).

Extracellular region or secreted Cytosol Plasma membrane Cytoskeleton Lysosome Endosome Peroxisome ER Golgi apparatus Nucleus Mitochondrion Manual annotation Automatic computational assertionSubcellular location
Tissue Specificity:

Predominant hexokinase isozyme expressed in insulin-responsive tissues such as skeletal muscle.

Subunit Structure:

Monomer (By similarity). Interacts with TIGAR; the interaction increases hexokinase activity in a hypoxia- and HIF1A-dependent manner.


The N- and C-terminal halves of the protein contain a hexokinase domain (PubMed:29298880). In contrast to hexokinase-1 and -3 (HK1 and HK3, respectively), both hexokinase domains display catalytic activity (PubMed:29298880). The region connecting the two hexokinase domains is required for the catalytic activity of the N-terminal hexokinase domain (PubMed:29298880). The N-terminal half regulates stability of the whole enzyme (PubMed:29298880).

Belongs to the hexokinase family.

Research Fields

· Environmental Information Processing > Signal transduction > HIF-1 signaling pathway.   (View pathway)

· Human Diseases > Endocrine and metabolic diseases > Type II diabetes mellitus.

· Human Diseases > Cancers: Overview > Central carbon metabolism in cancer.   (View pathway)

· Metabolism > Carbohydrate metabolism > Glycolysis / Gluconeogenesis.

· Metabolism > Carbohydrate metabolism > Fructose and mannose metabolism.

· Metabolism > Carbohydrate metabolism > Galactose metabolism.

· Metabolism > Carbohydrate metabolism > Starch and sucrose metabolism.

· Metabolism > Carbohydrate metabolism > Amino sugar and nucleotide sugar metabolism.

· Metabolism > Biosynthesis of other secondary metabolites > Neomycin, kanamycin and gentamicin biosynthesis.

· Metabolism > Global and overview maps > Metabolic pathways.

· Metabolism > Global and overview maps > Carbon metabolism.

· Organismal Systems > Endocrine system > Insulin signaling pathway.   (View pathway)

· Organismal Systems > Digestive system > Carbohydrate digestion and absorption.


1). α‑Phellandrene enhances the apoptosis of HT‑29 cells induced by 5‑fluorouracil by modulating the mitochondria‑dependent pathway. Oncology reports, 2024 (PubMed: 38456489) [IF=4.2]

Application: IF/ICC    Species: Human    Sample: HT-29 cells

Figure 3. Effect of α-PA combined with 5-FU treatment on VDAC-1 and HK-2 protein expression in HT-29 cells. HT-29 cells (1.0×105 cells/30-mm plate) were treated with 50, 100 or 250 µg/mM α-PA combined with 5-FU for 72 h. (A) Immunocytochemical staining was performed to determine the expression levels of HK-2 (green) and VDAC-1 (red) (Hoechst 33342 (blue) (×400 magnification). Quantitative analysis of the relative expression levels of (B) HK-2 and (C) VDAC-1 after treatment. Data are presented as the mean ± SD (n=3-5). *P

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