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The protein encoded by FH is an enzymatic component of the tricarboxylic acid (TCA) cycle, or Krebs cycle, and catalyzes the formation of L-malate from fumarate. Additionally we are shipping FH Antibodies (190) and FH Proteins (20) and many more products for this protein.
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We show that the mechanism of fumarate hydratase distribution is alternative transcription initiation from a broad promoter.
fumarate increases ferritin (show FTL ELISA Kits) gene transcription by activating the NRF2 (show GABPA ELISA Kits) (nuclear factor [erythroid-derived 2]-like 2) transcription factor.
FH-Ser75 phosphorylation level inversely correlates with the OGT (show OGT ELISA Kits) level and poor prognosis in pancreatic cancer patients. Report mechanism underlying transcription regulation by FH and the linkage between dysregulated OGT (show OGT ELISA Kits) activity and growth advantage of cancer cells under glucose deficiency.
Loss of FH immunohistochemical (IHC) expression in cutaneous leiomyomas is a sensitive and specific marker for detection of hereditary leiomyomatosis and renal cell carcinoma (HLRCC). FH expression by IHC was absent in 9 specimens and retained in 85 specimens and 2 cases were equivocal with minimal FH expression while succinate dehydrogenase B (show SDHB ELISA Kits) expression was retained in 95 specimens and equivocal in 1 specimen.
LSH (show HELLS ELISA Kits) promoted cancer progression in part by regulating expression of fumarate hydratase (FH).
Cascade FH mutation screening enabled the early diagnosis of a renal tumour in an asymptomatic parent of a child with fumarate hydratase deficiency, resulting in timely and possibly life-saving treatment.
Mutations in some enzymes of the TCA cycle: Isocitrate dehydrogenase (IDH (show IDH1 ELISA Kits)), succinate dehydrogenase (SDH (show SDHA ELISA Kits)) and fumarate hydratase (FH) are associated with the accumulation of metabolites that are able to influence many aspects of cancer development and progression and for this reason are termed onco-metabolites.
After indirect co-culture, OP was increased in the BxPc-3 and Panc-1 cells; correspondingly, succinate dehydrogenase (show SDHA ELISA Kits), FH and MCT expression were increased. After the MCT1 (show CMA1 ELISA Kits)-specific inhibitor removed 'tumor-stromal' metabolic coupling, the migration and invasion abilities of the pancreatic cancer cells were decreased.
A novel deletion of the Fumarate Hydratase (FH) gene was identified in a 22 year old male and his father, which predisposes to an aggressive form of renal cell cancer.
While the great majority of patients with hereditary leiomyomatosis and renal cell carcinoma will have FH-deficient leiomyomas, 1% of all uterine leiomyomas are FH deficient usually due to somatic inactivation.
roles for fumarate metabolism in hematopoietic stem cell (HSC) maintenance and hematopoietic differentiation and reveal a differential requirement for mitochondrial Fh1 in normal hematopoiesis and leukemia propagation.
Adipose-Specific Deficiency of Fumarate Hydratase in Mice Protects Against Obesity, Hepatic Steatosis, and Insulin (show INS ELISA Kits) Resistance.
Reexpression of cytosolic FH in FH1-deficient mice is critical for the suppression of renal cyst development and restoration of defects in the arginine biosynthesis pathway.
Tumor-derived FH and SDH (show SDS ELISA Kits) mutations accumulate fumarate and succinate, leading to enzymatic inhibition of multiple alpha-KG-dependent dioxygenases and consequent alterations of genome-wide histone and DNA methylation (show HELLS ELISA Kits).
identification of a metabolic pathway that is induced in Fh1-deficient cells to demonstrate that inhibition of haem oxygenation is synthetically lethal when combined with Fh1 deficiency, providing a new potential target for treating HLRCC patients
These experiments demonstrated that upregulation of HIF-1alpha (show HIF1A ELISA Kits) occurs as a direct consequence of FH inactivation.
progression of tumors where FH is lost might be boosted by activation of the MET oncogene (show RAB1A ELISA Kits), which is able to drive cell-autonomous tumor progression
The protein encoded by this gene is an enzymatic component of the tricarboxylic acid (TCA) cycle, or Krebs cycle, and catalyzes the formation of L-malate from fumarate. It exists in both a cytosolic form and an N-terminal extended form, differing only in the translation start site used. The N-terminal extended form is targeted to the mitochondrion, where the removal of the extension generates the same form as in the cytoplasm. It is similar to some thermostable class II fumarases and functions as a homotetramer. Mutations in this gene can cause fumarase deficiency and lead to progressive encephalopathy.
fumarate hydratase, mitochondrial
, fumarate hydratase
, fumarate hydratase 1