Proteintech

PFKL Monoclonal Antibody (1H2G2)

PFKL Antibody in Immunocytochemistry (ICC/IF)

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PFKL Antibody (68385-1-IG) in ICC/IF

Immunofluorescent analysis of (-20°C Methanol) fixed HuH-7 cells using PFKL antibody (68385-1-Ig, Clone: 1H2G2) at dilution of 1:800 and CoraLite®488-Conjugated Goat Anti-Mouse IgG (H+L).

PFKL Antibody in Immunohistochemistry (Paraffin) (IHC (P))

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Product Details

68385-1-IG

Applications

Tested Dilution

Publications

Western Blot (WB)

1:5,000-1:50,000

View 2 publications 2 publications

Immunohistochemistry (IHC)

View 2 publications 2 publications

Immunohistochemistry (Paraffin) (IHC (P))

1:1,000-1:4,000

Immunocytochemistry (ICC/IF)

1:400-1:1,600

View 2 publications 2 publications

Flow Cytometry (Flow)

0.80 µg/10^6 cells in a 100 µL suspension

View 2 publications 2 publications

ELISA (ELISA)

Assay-dependent

Product Specifications

Species Reactivity

Human, Mouse, Pig, Rabbit, Rat

Published species

Human, Mouse, Pig, Rabbit, Rat

Host/Isotype

Mouse / IgG1

Class

Monoclonal

Type

Antibody

Clone

1H2G2

Immunogen

PFKL fusion protein Ag8250

View immunogen

Conjugate

Unconjugated Unconjugated Unconjugated

Form

Liquid

Concentration

1 mg/mL

Purification

Protein G

Storage buffer

PBS, pH 7.3, with 50% glycerol

Contains

0.02% sodium azide

Storage conditions

-20°C

Shipping conditions

Wet ice

Product Specific Information

Immunogen sequence: TGISHGHTVY VVHDGFEGLA KGQVQEVGWH DVAGWLGRGG SMLGTKRTLP KGQLESIVEN IRIYGIHALL VVGGFEAYEG VLQLVEARGR YEELCIVMCV IPATISNNVP GTDFSLGSDT AVNAAMESCD RIKQSASGTK RRVFIVETMG GYCGYLATVT GIAVGADAAY VFEDPFNIHD LKVNVEHMTE KMKTDIQRGL VLRNEKCHDY YTTEFLYNLY SSEGNGVFDC RTNVLGHLQQ GGAPTPFDRN YGTKLGVKAM LWLSEKLREV YRKGRVFANA PDSACVIGLK KKAAAFSPVT ELKKDTDFEH RMPREQWWLS LRLMLKMLAQ YRISMAAYVS GELEHVTRRT LSMDKGF

Target Information

Phosphofructokinase (PFK), a major regulatory enzyme in all cells of the body, catalyzes the metabolism of sugar, and thereby is pivotal in the production of energy to maintain normal cell function. In human there are three structural loci controlling PFK: M (muscle), L (liver), and P (platelet) type subunits, which are variably expressed in different tissues; human diploid fibroblasts and leukocytes express all three genes. PFK, a tetramer formed by the random association of the products of two separate gene loci to form the five possible tetramers. PFKs of muscle and liver are homotetramers of the M and L subunits, respectively. Red cells have all five isozymes: M4, M3L, M2L2, ML3, and L4. PFK is an allosteric enzyme activated by ADP, AMP, or fructose bisphosphate and inhibited by ATP or citrate. PFK catalyzes the key controlling step of glycolytic pathway. PFK deficiency can present as mild to life-threatening episodic illness. A hallmark sign of this disease is intermittent dark urine, with the color of the urine ranging from orange to dark coffee-brown, which commonly develops following strenuous exercise. The mean red cell PFK is elevated in persons with Down syndrome.

For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.

Product References

Protein kinase N1 deficiency results in upregulation of cerebral energy metabolism and is highly protective in in vivo and in vitro stroke models.

Metabolism: clinical and experimental

Zur Nedden S,Safari MS,Weber D,Kuenkel L,Garmsiri C,Lang L,Orset C,Freret T,Haelewyn B,Hotze M,Kwiatkowski M,Sarg B,Faserl K,Savic D,Skvortsova II,Krogsdam A,Carollo S,Trajanoski Z,Oberacher H,Zlotek D,Ostermaier F,Cameron A,Baier G,Baier-Bitterlich G

Sun Dec 01 00:00:00 UTC 2024

Protein kinase N1 deficiency results in upregulation of cerebral energy metabolism and is highly protective in in vivo and in vitro stroke models.

Metabolism: clinical and experimental

Sun Dec 01 00:00:00 UTC 2024

Protein kinase N1 deficiency results in upregulation of cerebral energy metabolism and is highly protective in in vivo and in vitro stroke models.

Metabolism: clinical and experimental

Sun Dec 01 00:00:00 UTC 2024

Protein kinase N1 deficiency results in upregulation of cerebral energy metabolism and is highly protective in in vivo and in vitro stroke models.

Metabolism: clinical and experimental

Sun Dec 01 00:00:00 UTC 2024

Protein kinase N1 deficiency results in upregulation of cerebral energy metabolism and is highly protective in in vivo and in vitro stroke models.

Metabolism: clinical and experimental

Sun Dec 01 00:00:00 UTC 2024

Protein kinase N1 deficiency results in upregulation of cerebral energy metabolism and is highly protective in in vivo and in vitro stroke models.

Metabolism: clinical and experimental

Sun Dec 01 00:00:00 UTC 2024

Protein kinase N1 deficiency results in upregulation of cerebral energy metabolism and is highly protective in in vivo and in vitro stroke models.

Metabolism: clinical and experimental

Sun Dec 01 00:00:00 UTC 2024

Protein kinase N1 deficiency results in upregulation of cerebral energy metabolism and is highly protective in in vivo and in vitro stroke models.

Metabolism: clinical and experimental

Sun Dec 01 00:00:00 UTC 2024

Protein kinase N1 deficiency results in upregulation of cerebral energy metabolism and is highly protective in in vivo and in vitro stroke models.

Metabolism: clinical and experimental

Sun Dec 01 00:00:00 UTC 2024

Protein kinase N1 deficiency results in upregulation of cerebral energy metabolism and is highly protective in in vivo and in vitro stroke models.

Metabolism: clinical and experimental

Sun Dec 01 00:00:00 UTC 2024

Protein kinase N1 deficiency results in upregulation of cerebral energy metabolism and is highly protective in in vivo and in vitro stroke models.

Metabolism: clinical and experimental

Sun Dec 01 00:00:00 UTC 2024

Protein kinase N1 deficiency results in upregulation of cerebral energy metabolism and is highly protective in in vivo and in vitro stroke models.

Metabolism: clinical and experimental

Sun Dec 01 00:00:00 UTC 2024

Protein kinase N1 deficiency results in upregulation of cerebral energy metabolism and is highly protective in in vivo and in vitro stroke models.

Metabolism: clinical and experimental

Sun Dec 01 00:00:00 UTC 2024

Protein kinase N1 deficiency results in upregulation of cerebral energy metabolism and is highly protective in in vivo and in vitro stroke models.

Metabolism: clinical and experimental

Sun Dec 01 00:00:00 UTC 2024

Protein kinase N1 deficiency results in upregulation of cerebral energy metabolism and is highly protective in in vivo and in vitro stroke models.

Metabolism: clinical and experimental

Sun Dec 01 00:00:00 UTC 2024

Protein kinase N1 deficiency results in upregulation of cerebral energy metabolism and is highly protective in in vivo and in vitro stroke models.

Metabolism: clinical and experimental

Sun Dec 01 00:00:00 UTC 2024

Protein kinase N1 deficiency results in upregulation of cerebral energy metabolism and is highly protective in in vivo and in vitro stroke models.

Metabolism: clinical and experimental

Sun Dec 01 00:00:00 UTC 2024

Protein kinase N1 deficiency results in upregulation of cerebral energy metabolism and is highly protective in in vivo and in vitro stroke models.

Metabolism: clinical and experimental

Sun Dec 01 00:00:00 UTC 2024

Protein kinase N1 deficiency results in upregulation of cerebral energy metabolism and is highly protective in in vivo and in vitro stroke models.

Metabolism: clinical and experimental

Sun Dec 01 00:00:00 UTC 2024

Protein kinase N1 deficiency results in upregulation of cerebral energy metabolism and is highly protective in in vivo and in vitro stroke models.

Metabolism: clinical and experimental

Sun Dec 01 00:00:00 UTC 2024

Identification of hub glycolysis-related genes in acute myocardial infarction and their correlation with immune infiltration using bioinformatics analysis.

BMC cardiovascular disorders