Forgot Password

If you have forgotten your password you can enter your email here and get a temporary password sent to your email.

Calnexin - ER membrane marker antibody


Antibody ID


Target Antigen

Canx human, mouse

Proper Citation

(Abcam Cat# ab22595, RRID:AB_2069006)


polyclonal antibody


validation status unknown, seller recommendations provided in 2012:western blot, immunohistochemistry, immunocytochemistry

Host Organism




Cat Num


Publications that use this research resource

NADH Shuttling Couples Cytosolic Reductive Carboxylation of Glutamine with Glycolysis in Cells with Mitochondrial Dysfunction.

  • Gaude E
  • Mol. Cell
  • 2018 Feb 15

Literature context:


The bioenergetics and molecular determinants of the metabolic response to mitochondrial dysfunction are incompletely understood, in part due to a lack of appropriate isogenic cellular models of primary mitochondrial defects. Here, we capitalize on a recently developed cell model with defined levels of m.8993T>G mutation heteroplasmy, mTUNE, to investigate the metabolic underpinnings of mitochondrial dysfunction. We found that impaired utilization of reduced nicotinamide adenine dinucleotide (NADH) by the mitochondrial respiratory chain leads to cytosolic reductive carboxylation of glutamine as a new mechanism for cytosol-confined NADH recycling supported by malate dehydrogenase 1 (MDH1). We also observed that increased glycolysis in cells with mitochondrial dysfunction is associated with increased cell migration in an MDH1-dependent fashion. Our results describe a novel link between glycolysis and mitochondrial dysfunction mediated by reductive carboxylation of glutamine.

Funding information:
  • NIAID NIH HHS - K08 AI076429-03(United States)

GDC-0879, a BRAFV600E Inhibitor, Protects Kidney Podocytes from Death.

  • Sieber J
  • Cell Chem Biol
  • 2018 Feb 15

Literature context:


Progressive kidney diseases affect approximately 500 million people worldwide. Podocytes are terminally differentiated cells of the kidney filter, the loss of which leads to disease progression and kidney failure. To date, there are no therapies to promote podocyte survival. Drug repurposing may therefore help accelerate the development of cures in an area of tremendous unmet need. In a newly developed high-throughput screening assay of podocyte viability, we identified the BRAFV600E inhibitor GDC-0879 and the adenylate cyclase agonist forskolin as podocyte-survival-promoting compounds. GDC-0879 protects podocytes from injury through paradoxical activation of the MEK/ERK pathway. Forskolin promotes podocyte survival by attenuating protein biosynthesis. Importantly, GDC-0879 and forskolin are shown to promote podocyte survival against an array of cellular stressors. This work reveals new therapeutic targets for much needed podocyte-protective therapies and provides insights into the use of GDC-0879-like molecules for the treatment of progressive kidney diseases.

Funding information:
  • NIDDK NIH HHS - R01 DK095045()
  • NIDDK NIH HHS - R01 DK099465()
  • NINDS NIH HHS - 4R00NS057944-03(United States)

Organelle Specific O-Glycosylation Drives MMP14 Activation, Tumor Growth, and Metastasis.

  • Nguyen AT
  • Cancer Cell
  • 2017 Nov 13

Literature context:


Cancers grow within tissues through molecular mechanisms still unclear. Invasiveness correlates with perturbed O-glycosylation, a covalent modification of cell-surface proteins. Here, we show that, in human and mouse liver cancers, initiation of O-glycosylation by the GALNT glycosyl-transferases increases and shifts from the Golgi to the endoplasmic reticulum (ER). In a mouse liver cancer model, expressing an ER-targeted GALNT1 (ER-G1) massively increased tumor expansion, with median survival reduced from 23 to 10 weeks. In vitro cell growth was unaffected, but ER-G1 strongly enabled matrix degradation and tissue invasion. Unlike its Golgi-localized counterpart, ER-G1 glycosylates the matrix metalloproteinase MMP14, a process required for tumor expansion. Together, our results indicate that GALNTs strongly promote liver tumor growth after relocating to the ER.