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Literature summary for 2.1.2.1 extracted from

  • Kim, D.; Fiske, B.P.; Birsoy, K.; Freinkman, E.; Kami, K.; Possemato, R.L.; Chudnovsky, Y.; Pacold, M.E.; Chen, W.W.; Cantor, J.R.; Shelton, L.M.; Gui, D.Y.; Kwon, M.; Ramkissoon, S.H.; Ligon, K.L.; Kang, S.W.; Snuderl, M.; Vander Heiden, M.G.; Sabatini, D.M.
    SHMT2 drives glioma cell survival in ischaemia but imposes a dependence on glycine clearance (2015), Nature, 520, 363-367.
    View publication on PubMedView publication on EuropePMC

Cloned(Commentary)

Cloned (Comment) Organism
gene SHMT2, expression analysis Homo sapiens

Localization

Localization Comment Organism GeneOntology No. Textmining
mitochondrion
-
Homo sapiens 5739
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Organism

Organism UniProt Comment Textmining
Homo sapiens P34897
-
-

Source Tissue

Source Tissue Comment Organism Textmining
0308 cell expresses low levels of SHMT2 Homo sapiens
-
brain in healthy brains, SHMT2 expression is not detected in most cells but is at low levels in astrocytes and vessels Homo sapiens
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BT-145 cell expresses low levels of SHMT2 Homo sapiens
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glioblastoma cell in human glioblastoma multiforme, mitochondrial serine hydroxymethyltransferase (SHMT2) and glycine decarboxylase are highly expressed in the pseudopalisading cells that surround necrotic foci Homo sapiens
-
glioma cell expression of SHMT2 in ischemic tumor zones Homo sapiens
-
LN-229 cell
-
Homo sapiens
-
pseudopalisading cell
-
Homo sapiens
-
U-251 cell
-
Homo sapiens
-

Synonyms

Synonyms Comment Organism
mitochondrial serine hydroxymethyltransferase
-
Homo sapiens
SHMT2
-
Homo sapiens

General Information

General Information Comment Organism
malfunction suppression of SHMT2 decreases both net serine consumption and glycine production in LN229 cells and completely prevents glycine cleavage activity in isolated mitochondria. The preemptive knockdown of SHMT2 protects BT145, LN229, and U251 cells against the detrimental effects of GLDC knockdown Homo sapiens
metabolism key role for serine and glycine metabolism in the survival of brain cancer cells within the ischemic zones of gliomas. Glycine decarboxylase inhibition impairs cells with high SHMT2 levels as the excess glycine not metabolized by glycine decarboxylase can be converted to the toxic molecules aminoacetone and methylglyoxal. SHMT2 activity limits that of pyruvate kinase (PKM2) and reduces oxygen consumption, eliciting a metabolic state that confers a profound survival advantage to cells in poorly vascularized tumor regions Homo sapiens
physiological function SHMT2 is required for cancer cells to adapt to the tumor environment, but also renders these cells sensitive to glycine cleavage system inhibition. The enzyme has a key role in cells in environments with limited oxygen or nutrient levels Homo sapiens