Paul Kaminski
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paulkaminski95.bsky.social
Paul Kaminski
@paulkaminski95.bsky.social
MD/PhD Student @UPenn
Interested in epigenetics & blood disorders
Reposted by Paul Kaminski
Bluetorial-Jim Watson

I met Jim Watson a few times but did not know him well. However, I was greatly influenced by his book “The Double Helix”. He was a complicated human being with some very, very bad features, but some good contributions.

What follows is my personal perspective.

1/41
a cartoon says hey everybody an old man 's talking while bart simpson looks on
ALT: a cartoon says hey everybody an old man 's talking while bart simpson looks on
media.tenor.com
November 8, 2025 at 1:58 PM
Reposted by Paul Kaminski
Our latest paper has just been published in Cell!

doi.org/10.1016/j.ce...

We developed a new method called MCC ultra, which allows 3D chromatin structure to be visualised with a 1 base pair pixel size.
November 5, 2025 at 5:20 PM
Reposted by Paul Kaminski
1/ 🚀 AEBP2 isn’t what we thought.

You were told that AEBP2 promotes PRC2 activity on chromatin.

We found the opposite: the most prevalent AEBP2 isoform inhibits PRC2 activity.

👉 surl.li/cgwqcq

A thread 🧵
October 31, 2025 at 10:53 AM
Reposted by Paul Kaminski
🧵1/Exciting news in cancer epigenetics! Our latest research, "AEBP2-Directed H3K27me2 Defines a Specific Vulnerability in EZH2-mutant Lymphoma", is now available on www.biorxiv.org/content/10.1.... Here's a thread summarizing our findings!👇
#CancerResearch #Epigenetics #Chromatin #Lymphoma
AEBP2-Directed H3K27me2 Defines a Specific Vulnerability in EZH2-mutant Lymphoma
The catalytic subunit of Polycomb Repressive Complex 2 (PRC2), EZH2, is recurrently mutated in 25% of diffuse large B-cell lymphomas (DLBCL), causing increased H3K27me3 and decreased H3K27me2 levels. ...
www.biorxiv.org
October 17, 2025 at 7:11 AM
Reposted by Paul Kaminski
Check it out, Chromatin Kids!

Chromatin remodeller does stuff to Transcription Factors!

Functions where it is seldom seen!

Both decreases and increases chromatin accessibility!

How cool is that?
The chromatin remodeller CHD4 controls both nucleosome integrity and transcription factor binding to promote activity of active regulatory elements and to prevent activation of silent enhancers https://www.biorxiv.org/content/10.1101/2025.08.29.672645v1
August 30, 2025 at 4:18 PM
Reposted by Paul Kaminski
Excited to share a new preprint from the lab!

This (doi.org/10.1101/2025...) and an earlier one (doi.org/10.1101/2025...) mark my lab's first steps into studying how Polycomb modifications get established in early Drosophila development.
🧵 1/10
Lower-order methylation states underlie the maintenance and re-establishment of Polycomb modifications in Drosophila embryogenesis https://www.biorxiv.org/content/10.1101/2025.07.25.666882v1
July 29, 2025 at 11:36 PM
Reposted by Paul Kaminski
We are excited to share our new preprint demonstrating that nucleic acid interactions with SUZ12 constrain PRC2 activity, establishing a kinetic buffer essential for targeted gene silencing and revealing vulnerabilities in diffuse midline gliomas.
www.biorxiv.org/content/10.1...
July 23, 2025 at 11:38 PM
Reposted by Paul Kaminski
Another paper bluetorial! Today: how does the spatial location of genes influence their function? (1/n) www.nature.com/articles/s41...
The nuclear periphery confers repression on H3K9me2-marked genes and transposons to shape cell fate - Nature Cell Biology
Marin et al. report the role of lamin proteins and the lamin B receptor (LBR) in chromatin positioning at the nuclear periphery. Knockout of all lamins and LBR in mouse embryonic stem cells leads to h...
www.nature.com
July 22, 2025 at 5:10 PM
Reposted by Paul Kaminski
[0/8] Stoked to share our work with @arjunraj.bsky.social on tissue organization in the gastruloid. We use lineage tracing and spatial transcriptomics to show that diversity among stem cell clones promotes, rather than hinders, gastruloid development: www.biorxiv.org/content/10.1...
Gastruloid patterning reflects division of labor among biased stem cell clones
Embryonic development typically requires precise coordination among cells to achieve reproducible outcomes, leading to the assumption that cellular heterogeneity must be minimized or buffered against....
www.biorxiv.org
July 15, 2025 at 3:44 PM
Reposted by Paul Kaminski
Online Now: CRAMP1 drives linker histone expression to enable Polycomb repression Online now:
CRAMP1 drives linker histone expression to enable Polycomb repression
Challenging the prevailing view that H1 linker histones represent a general feature of repressed chromatin, Matthews et al. show a specific requirement for H1 in epigenetic repression by PRC2. Ablation of the H1 activator CRAMP1 results in linker histone insufficiency and derepression of PRC2 target genes.
dlvr.it
June 13, 2025 at 7:14 PM
Reposted by Paul Kaminski
New from our lab & @harrisonflylab.bsky.social: Drosophila models of H3 K27M & EZHIP reveal conserved chromatin regulators that buffer PRC2 inhibition. An in vivo screen highlights how developmental defects can be rescued despite global H3K27me3 loss.
doi.org/10.1101/2025...
May 27, 2025 at 3:29 PM
Reposted by Paul Kaminski
I'm genuinely sorry that Fetterman had a stroke and suffers from depression. But arguing that he has a free pass not to do his job in the name of destigmatizing brain injury and mental health struggles is offensive. If he can't do it, he should resign. If he doesn't want to, he should resign faster.
In which John Fetterman argues with inflamed self-righteousness that he's being bullied into doing parts of the job that he thinks are dumb. Like...showing up to vote. And serving on Senatorial committees. And meeting with constituents. www.nytimes.com/2025/05/24/u...
Fetterman, Often Absent From Senate, Says He Has Been Shamed Into Returning
www.nytimes.com
May 24, 2025 at 10:11 PM
Reposted by Paul Kaminski
Online Now: A specific form of cPRC1 containing CBX4 is co-opted to mediate oncogenic gene repression in diffuse midline glioma Online now:
A specific form of cPRC1 containing CBX4 is co-opted to mediate oncogenic gene repression in diffuse midline glioma
Lagan, Gannon, et al. reveal that H3K27M-DMGs depend on a specific form of cPRC1 containing CBX4 and PCGF4. H3K27M alters H3K27me3 distribution, causing increased binding of CBX4-PCGF4-cPRC1 and oncogenic gene repression. CBX4’s ability to read H3K27me3 and to form a specific cPRC1 complex with PCGF4 makes it essential in DMG.
dlvr.it
May 21, 2025 at 3:19 PM
Reposted by Paul Kaminski
I shared the story of Natalie, a mom from WA state with stage 4 colorectal cancer enrolled in an NIH clinical trial, but she was told her care was delayed because of RFK Jr.'s staffing cuts.

He admitted NIH cuts, "are gonna hurt."
 
It's unacceptable. I'm demanding accountability.
"NIH Cuts Will Hurt" RFK Jr. Admits When Pressed by Senator Murray on Harm to NIH Clinical Care
YouTube video by Senator Patty Murray
www.youtube.com
May 14, 2025 at 9:03 PM
Reposted by Paul Kaminski
This cure for sickle cell anemia was made possible by NIH-funded research to turn the gene for fetal hemoglobin back on. It was done predominantly by NIH researchers, including intramural researchers on the NIH campus.

irp.nih.gov/catalyst/33/...
March 15, 2025 at 6:44 PM
Reposted by Paul Kaminski
1/ H3K27me3 mimicry has repeatedly emerged through evolution, but what's the physiological relevance?

We show that JARID2 and PALI1 mimic H3K27me3 to antagonise PRC2 in vivo and restrict the spread of Polycomb domains.
🧵
www.biorxiv.org/content/10.1...
March 15, 2025 at 12:12 AM
Reposted by Paul Kaminski
Reposted by Paul Kaminski
Why does National Institutes of Health funding matter? It’s the fuel to find cures for:

- Cancer
- Alzheimer’s
- Cystic Fibrosis
- Pediatric Cancer
- ALS
- MS
- Parkinson’s

Trump tried to cut it, but thanks to AG Campbell, a judge blocked the cuts. This is why we fight.
February 26, 2025 at 4:09 PM
Reposted by Paul Kaminski
Online now: Online Now: EZH1/EZH2 inhibition enhances adoptive T cell immunotherapy against multiple cancer models
EZH1/EZH2 inhibition enhances adoptive T cell immunotherapy against multiple cancer models
Porazzi et al. highlight how inhibiting the epigenetic regulators EZH2 and EZH1 enhances cancer cell immunogenicity, boosting the effectiveness of CAR- and TCR-engineered T cells across liquid and solid tumor models, which represents a promising strategy…
dlvr.it
February 20, 2025 at 7:51 PM
Reposted by Paul Kaminski
𝐇𝐨𝐰 𝐝𝐨 𝐜𝐞𝐥𝐥𝐬 𝐫𝐞𝐦𝐞𝐦𝐛𝐞𝐫 𝐰𝐡𝐨 𝐭𝐡𝐞𝐲 𝐚𝐫𝐞 𝐚𝐟𝐭𝐞𝐫 𝐃𝐍𝐀 𝐫𝐞𝐩𝐥𝐢𝐜𝐚𝐭𝐢𝐨𝐧? Our new study “Disabling leading and lagging strand histone transmission results in parental histones loss and reduced cell plasticity and viability” is out in 𝘚𝘤𝘪𝘦𝘯𝘤𝘦 𝘈𝘥𝘷𝘢𝘯𝘤𝘦𝘴. Led by @lleonie.bsky.social @biranalva.bsky.social 🧵 More below👇
Disabling leading and lagging strand histone transmission results in parental histones loss and reduced cell plasticity and viability
Losing parental histones during DNA replication fork passage challenges differentiation competence and cell viability.
tinyurl.com
February 19, 2025 at 7:35 PM
Reposted by Paul Kaminski
Trump & Musk are making massive cuts to the National Institutes of Health.

I know there is a lot going on right now, but this is one of worst things they have done so far, will affect cancer research and trials, the search for cures, innovation and competitiveness, our universities. Your lives.
February 8, 2025 at 11:16 PM
Reposted by Paul Kaminski
Congratulations to Eugene Khandros (@ChildrensPhila/ @pennmedicine.bsky.social) on being named a 2025 @the-asci.bsky.social Young Physician-Scientist Awardee! tinyurl.com/4472xuht Learn more about Dr. Khandros & his work here➡️ tinyurl.com/3x7bxehm
February 6, 2025 at 8:14 PM
Reposted by Paul Kaminski
Scientific advancements aside, this is economically irresponsible

Every $1 spent by NIH generates $2.46

For example, in 2023, $47B in NIH spending generated ~$93B

Halting NIH spending will LOSE the US a lot of money (and talent)
January 22, 2025 at 11:04 PM
Reposted by Paul Kaminski
Please see 🧵by @evhealy.bsky.social about our new paper exploring the role of PRC1 and PRC2 in non-dividing cells 👇
🧵 1/ We’re excited to share that our new paper with @adrianbracken.bsky.social lab is out 🎉 In this study (which began over 10 years ago!), we explore the biology of PRC2 and PRC1 in non-dividing cells. We also explore the effects of PRC2 inhibitor drugs on these cells. Here’s what we found👇
January 14, 2025 at 11:03 PM