#PCK1
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alicefrolov.bsky.social
Diverging log-scale lollipop chart ranking 54 tissues by PCK1 median expression relative to the cross-tissue median of 0.5 TPM, with tissues on one axis and fold difference on the other.

#Gluconeogenesis #PCK1 #GTEx #TumorMetabolism #HepaticMetabolism #MetabolicReprogramming #TissueTranscriptomics
I would like to share a visualization of PCK1 (phosphoenolpyruvate carboxykinase 1, cytosolic; GENCODE ENSG00000124253.10) expression across human tissues, with the aim of discussing how gluconeogenic capacity is distributed relative to cancer-relevant tissues. The figure is a diverging log-scale lollipop chart in which each tissue is ranked by its deviation from the cross-tissue median. The data are GTEx v8 median gene expression by tissue across 54 tissues, and these are bulk-tissue medians from postmortem donors, so cell-type composition differs between tissues. The cross-tissue median is 0.5 TPM (dashed line). Liver is the clear upper outlier at 530.0 TPM, which is 1052.7 times the median. At the other extreme, cultured fibroblasts show the lowest median at 0.04 TPM. A log axis is necessary here, because on a linear scale almost every tissue would collapse onto the baseline beside the hepatic value. Several points seem worth discussing. First, the magnitude of the hepatic signal is consistent with PCK1 being a core component of the hepatocyte gluconeogenic program, and high transcript abundance is associated with tissues that carry out net glucose production. Second, the very low values in cultured fibroblasts indicate that transcript abundance in this in vitro setting is far below the tissue median, which is relevant when PCK1 is interrogated in cell line models. Third, for tumor biology, a cancer-relevant tissue reading near or below the median is compatible with low basal PCK1 transcription, but bulk medians cannot resolve whether this reflects epithelial, stromal or immune contributions. Important limitations: TPM medians do not report enzymatic flux, protein abundance or post-translational regulation, and donor-level variance is not shown in this summary view. Matched tumor-normal comparisons would be needed before drawing any inference about metabolic rewiring in malignancy. I would like to share a visualization of PCK1 (phosphoenolpyruvate carboxykinase 1, cytosolic; GENCODE ENSG00000124253.10) expression across human tissues, with the aim of discussing how gluconeogenic capacity is distributed relative to cancer-relevant tissues. The figure is a diverging log-scale lollipop chart in which each tissue is ranked by its deviation from the cross-tissue median. The data are GTEx v8 median gene expression by tissue across 54 tissues, and these are bulk-tissue medians from postmortem donors, so cell-type composition differs between tissues. The cross-tissue median is 0.5 TPM (dashed line). Liver is the clear upper outlier at 530.0 TPM, which is 1052.7 times the median. At the other extreme, cultured fibroblasts show the lowest median at 0.04 TPM. A log axis is necessary here, because on a linear scale almost every tissue would collapse onto the baseline beside the hepatic value. Several points seem worth discussing. First, the magnitude of the hepatic signal is consistent with PCK1 being a core component of the hepatocyte gluconeogenic program, and high transcript abundance is associated with tissues that carry out net glucose production. Second, the very low values in cultured fibroblasts indicate that transcript abundance in this in vitro setting is far below the tissue median, which is relevant when PCK1 is interrogated in cell line models. Third, for tumor biology, a cancer-relevant tissue reading near or below the median is compatible with low basal PCK1 transcription, but bulk medians cannot resolve whether this reflects epithelial, stromal or immune contributions. Important limitations: TPM medians do not report enzymatic flux, protein abundance or post-translational regulation, and donor-level variance is not shown in this summary view. Matched tumor-normal comparisons would be needed before drawing any inference about metabolic rewiring in malignancy.
November 4, 2026 at 5:02 PM
sanaprohini.bsky.social
www.linkedin.com/pulse/pck1-a...
Pck1 Antibody Market: US, Japan, Korea, Europe Analysis and Future Outlook
The Pck1 Antibody Market was valued at USD 1.2 Billion in 2025 and is poised to grow from USD 1.
www.linkedin.com
October 28, 2026 at 6:54 AM
asimresearcher.bsky.social
Redox-driven PCK1 sulfenylation: An early warning signal for progression from metabolically healthy obesity to diabetes https://pubmed.ncbi.nlm.nih.gov/42860109/
October 12, 2026 at 10:21 AM
shakiramrfr.bsky.social
Size of the PCK1 antibody market and future growth... | WiseGuyReports www.wiseguyreports.com/de/reports/p...
www.wiseguyreports.com
October 2, 2026 at 3:24 PM
purpleswallowarts.bsky.social
Any holiday is a good time to send a greeting your favorite Taiji Animal notecard 📬https://purpleswallowarts.com/shop/ols/products/four-card-variety-pack-fr-crd-vrt-pck1
2nd Edition - Four Card Variety Pack
One each of four designs of Taiji inspired notecard with posture name and animal on front. Interior contains a poetic message connected to the posture. Printed from my original artwork on 65lb Sweet T...
purpleswallowarts.com
September 28, 2026 at 8:12 PM
plant-sci.bsky.social
🌱🧬Brassinosteroids promote sugar synthesis by activating PCK1 via dephosphorylation. BIN2 kinase phosphorylates PCK1, inhibiting it. BRs lift this brake, boosting gluconeogenesis and photosynthesis

A hormone–metabolism link with growth implications. #plantscience
www.nature.com/articles/s41...
Brassinosteroids promote sugar synthesis by inhibiting BIN2 phosphorylation of phosphoenolpyruvate carboxykinase - Nature Plants
Whether growth-promoting hormones boost sugar synthesis has remained unclear. Brassinosteroids were found to do so by relieving BIN2-mediated inhibition of PCK1, a key enzyme in gluconeogenesis and ph...
www.nature.com
September 2, 2026 at 8:55 AM
natplants.nature.com
New OA Article: "Brassinosteroids promote sugar synthesis by inhibiting BIN2 phosphorylation of phosphoenolpyruvate carboxykinase" rdcu.be/Q5Fqmnw1EPna

BRs were found to relieve BIN2-mediated inhibition of PCK1, a key enzyme in gluconeogenesis and photosynthesis. #PlantScience
August 31, 2026 at 12:09 PM
tohoku-life-news-j.bsky.social
（続き）

BR シグナルの抑制因子であるBIN2 キナーゼ （注3） が、糖新生の鍵酵素PCK1 （注4） の特定部位をリン酸化し、酵素の立体構造を6 量体から12 量体へ変化させることで、その働きを強く阻害することを発見しました。 この制御機構は、発芽直後の実生定着における糖新生だけでなく、トウモロコシやソルガムなどC4 植物 （注5） の特殊な光合成においても重要な役割を果たしており、将来的な作物のバイオマス生産向上に向けた新たな標的として期待されます。
August 31, 2026 at 10:59 AM
yokoyama-ryo.bsky.social
Brassinosteroids promote sugar synthesis by inhibiting BIN2 phosphorylation of phosphoenolpyruvate carboxykinase www.nature.com/articles/s41... @natplants.nature.com
Brassinosteroids promote sugar synthesis by inhibiting BIN2 phosphorylation of phosphoenolpyruvate carboxykinase - Nature Plants
Whether growth-promoting hormones boost sugar synthesis has remained unclear. Brassinosteroids were found to do so by relieving BIN2-mediated inhibition of PCK1, a key enzyme in gluconeogenesis and ph...
www.nature.com
August 28, 2026 at 11:19 AM
jimd-editors.bsky.social
New case report in JIMD Reports:
A novel PCK1 variant causing cytosolic PEPCK deficiency in two siblings, with dramatically different phenotypes, including reversible acute liver failure.

Hyperglutaminemia + normal ammonia = key diagnostic clue.

doi.org/10.1002/jmd2...

#RareDisease #IMD #PCK1
February 2, 2026 at 5:32 AM
lifespannews.bsky.social
In a recent study, researchers have described how one of the core enzymes involved in metabolism is required to stave off senescence in fat (adipose) cells.

lifespan.io/news/how-an-...
By: Josh Conway
How an Enzyme’s Depletion Makes Fat Worse
In Aging Cell, researchers have described how the enzyme Pck1, a core part of metabolic activity, is required for staving off senescence in fat (adipose) cells.
lifespan.io
April 2, 2026 at 5:31 PM
prepub-singlecell.bsky.social
Ablation of the Renal Tubular Gluconeogenic Enzyme PCK1 Drives AKI-to-CKD Transition by Negatively Regulating the TGF-β/Smad3 Signaling Pathway #SingleCell 🧪🧬🖥️
https://www.researchsquare.com/article/rs-9202714/latest
April 2, 2026 at 7:00 AM
tzx21.bsky.social
@pck1.bsky.social
September 4, 2024 at 1:13 PM
tkozawa.bsky.social
Great preprint by Zhang, Aizezi et al. (2025) on how #brassinosteroids promote phosphoenolpyruvate carboxykinase (PCK) activity for sugar synthesis in C3 and C4 plants, by inhibiting BIN2-mediated PCK phosphorylation at two conserved residues (Ser-62 and Thr-66). 🌱🌽

www.biorxiv.org/content/10.1...
Fig. 8: Summary of the roles of BIN2-PCK1 regulatory module in Arabidopsis and sorghum/maize. a) Brassinolide activates PCK1, by inhibiting BIN2 phosphorylation, to promote the conversion of lipids into sugar for Arabidopsis seedling establishment. b) BR and light regulate PCK1 in bundle sheath cells (BSC) for photosynthesis in sorghum and maize. CO2 is fixed by PEP carboxylase (PEPC) to make OAA in mesophyll cells (MC). OAA is then converted to Asp and transported to BSC, where OAA is decarboxylated by PCK1, thus releasing CO2 for photosynthesis. PEP returns to the MC for the next round of C4 cycle.
October 27, 2025 at 8:40 PM
joshuamurraynevill.bsky.social
If you'd like to see what modern, polished, corporate segregation looks like then prep yourself for some supremely creepy stuff.
www.youtube.com/watch?v=Pck1...
Black Man Investigates South Africa’s Whites-Only Town
YouTube video by Wide Awake Podcast
www.youtube.com
March 21, 2025 at 10:29 AM
kidneyint.bsky.social
Commentary
Round and round we go: phosphoenolpyruvate carboxykinase 1 (PCK1) in cataplerosis, mitochondrial, and kidney health

Mitchell A Sullivan and Josephine M Forbes

doi.org/10.1016/j.kint.2025.08.006

Original article: doi.org/10.1016/j.kint.2025.06.018

#NephSky #MedSky #kidneydisease
November 20, 2025 at 7:13 PM
rridrobot.bsky.social
RRID:AB_2878014 from @proteintech.bsky.social was used by authors in their Cell Reports paper. Thanks for making your methods matter! #RRID #ReproducibleResearch #methodsmatter
SEPHS2 loss reprograms cancer metabolism from oxidative phosphorylation to gluconeogenesis via PCK1 stabilization
Read the full paper: SEPHS2 loss reprograms cancer metabolism from oxidative phosphorylation to gluconeogenesis via PCK1 stabilization
doi.org
April 30, 2026 at 7:00 AM
rridrobot.bsky.social
The authors included RRIDs in their in Cell Metabolism paper! We value the author's support of reproducibility. #OpenScience #accelerateopenscience #reproducibility
Lack of PCK1 in hepatic stellate cells causes liver fibrosis by fueling tricarboxylic acid cycle and increasing glycolysis
Read the full paper: Lack of PCK1 in hepatic stellate cells causes liver fibrosis by fueling tricarboxylic acid cycle and increasing glycolysis
doi.org
February 26, 2026 at 7:47 PM
rridrobot.bsky.social
TKG's resource, RRID:CVCL_0470, was just reported to be used in "Suppression of PCK1 attenuates neuronal injury and improves post-resuscitation outcomes". We appreciate the author's support of reproducibility. #ReproducibleResearch #OpenScience
doi.org
February 1, 2025 at 8:01 AM
vulpineexpress.bsky.social
Man. I just found out The Chief of ACME passed away.
www.youtube.com/watch?v=Pck1...
Where In The World Is Carmen Sandiego? (1996) The Chief - Introduction
YouTube video by Yoshikarter1
www.youtube.com
June 13, 2025 at 8:07 PM
sciencedaily.com.web.brid.gy
Two common drugs could reverse fatty liver disease
Researchers at the University of Barcelona found that combining pemafibrate and telmisartan significantly reduces liver fat and cardiovascular risks in MASLD models. The drug duo works better together than alone, likely due to complementary mechanisms. They also uncovered a new role for the PCK1 protein in fat metabolism.
www.sciencedaily.com
October 12, 2025 at 7:41 PM
longtail-news.bsky.social
Feed: "Latest Science News -- ScienceDaily"
Published on Sunday, October 12, 2025
Two common drugs could reverse fatty liver disease
Researchers at the University of Barcelona found that combining pemafibrate and telmisartan significantly reduces liver fat and cardiovascular risks in MASLD models. The drug duo works better together than alone, likely due to complementary mechanisms. They also uncovered a new role for the PCK1 protein in fat metabolism.
www.sciencedaily.com
October 12, 2025 at 4:38 PM
cp-cellmetabolism.bsky.social
Online now: Lack of PCK1 in hepatic stellate cells causes liver fibrosis by fueling tricarboxylic acid cycle and increasing glycolysis
Lack of PCK1 in hepatic stellate cells causes liver fibrosis by fueling tricarboxylic acid cycle and increasing glycolysis
This study shows that a key metabolic enzyme, PCK1, protects the liver from scarring by keeping fibrogenic cells in a quiescent state. When PCK1 is reduced, these cells undergo metabolic reprogramming characterized by increased glycolysis, become aberrantly activated, and promote liver fibrosis in mice.
dlvr.it
February 23, 2026 at 4:42 PM