#transcription factor

[bpod-bpod]

Cardiac Mechanic

Biomechanical forces sculpt tissue during development: this study in zebrafish shows that a protein (transcription factor) called egr3 is vital for sensing such forces, turning them into molecular cellular signals regulating the development of heart valves

Read the published research article here

Image from work by Agatha Ribeiro da Silva and colleagues

Max Planck Institute for Heart and Lung Research, Department of Developmental Genetics, Bad Nauheim, Germany

Image originally published with a Creative Commons Attribution 4.0 International (CC BY 4.0)

Published in Science Advances, May 2024

You can also follow BPoD on Instagram, Twitter and Facebook

[medicomunicare]

AP-1: a keymaster FOStering the JUNction among several tissues by wERKing on the MAPk

AP-1: ID and biological functions AP-1 (Activator Protein-1) is a transcription factor that plays a key role in regulating gene expression involved in a wide range of cellular processes, including proliferation, apoptosis, differentiation and stress response. AP-1 is a protein complex composed mainly of members of the Fos (c-Fos, FosB, Fra-1, Fra-2) and Jun (c-Jun, JunB, JunD) protein families,…

[tenth-sentence]

The heat shock response appears to be mediated by one or more signal transduction pathways, one of which involves a specific set of transcription factors, called heat shock factors, that regulate the transcription of HSP mRNAs.

"Plant Physiology and Development" int'l 6e - Taiz, L., Zeiger, E., Møller, I.M., Murphy, A.

[whats-in-a-sentence]

For example, evolution has recruited the same transcription factor, APETALA2, to first regulate floral meristem identity and then floral organ identity (Table 20.3). (...) In Arabidopsis, LEAFY (LFY), FLOWERING D (FD), SUPPRESSOR OF OVEREXPRESSION OF CONSTANS1 (SOC1), and APETALA1 (AP1) are among the critical genes in the genetic pathway that must be activated to establish floral meristem identity (see Table 20.3). (...) Many of the genes that determine the floral organ identity are MADS box genes, including the DEFICIENS gene of snapdragon and the AGAMOUS (AG), PISTILLATA (PI), and APETALA3 (AP3) genes of Arabidopsis (see Table 20.3).

"Plant Physiology and Development" int'l 6e - Taiz, L., Zeiger, E., Møller, I.M., Murphy, A.

[noahtally-famous]

funny how this fic started off as an "unserious" idea (not cracky, more so i didn't take it that seriously, it was basically so i could rotate certain characters from my head into a google doc), i didn't expect to care abt it as much as i do now like i have a basic chapter layout for half of the set chapter count, specific scenes prewritten, a planning doc with around five pages thus far, the basics (title, summary, etc), random scenes for it spinning around in my head, and a bit of chapter one and three pages of chapter four written 😭

and i started properly thinking stuff for and working on this fic like...two days ago

it was not supposed to be This Serious hfjkdhf

[seventh-district]

not even gonna tag this properly bc i don't wanna get Involved but i do have some Thoughts i need to get out into the void so here we go

(aaa quick edit: CW for mention/discussion of Boothill leaks)

[theresa-of-liechtenstein]

well. ok then :/

[martyrbat]

fine... downloading batman 66 episodes and writing the transcripts as we speak. just for you guys (gn) <3

[unopenablebox]

thinking about goosecoid again

[grison-in-space]

This. This is exactly how I feel about fMRI and why I hate it so much. I mean, it doesn't help that I trained in EEB-style neuroscience so I default to wanting to know about differential gene expression and receptor expression patterns and knowing exactly what proteins are doing what when and how, none of which fMRI is ever going to show you: it's explicitly a technique that is all about the blood flow changes, and there's quite a lot of types of activity that can't be captured by that. Not to mention assumptions about blood flow matching 1:1 with activity. Like, cFOS drives me nuts, too—I have sharply asked SO MANY PEOPLE to tell me what the cFOS protein actually DOES in neuroscience settings and gotten a wide array of blank and terrified stares—but at least you actually are looking at a fucking protein there.

I just want to know what the cells are doing and how they're interacting with various signaling networks on the fly. Opto techniques work fairly well for that but for fairly obvious reasons (they involve either working with germ-line genetically modified subjects or injecting retroviruses designed to modify gene expression directly into the brain) they're not great for human use.

Any time sometime uses "activation" to refer to a brain, though, you march up to them and you ask exactly what "activated" means in this context anyway. There are at least half a dozen things people collapse under that term and they really, really oughtn't.

one of the best academic paper titles

[bpod-bpod]

Reprogramming Scars

After a heart attack, cardiac fibroblasts (shown) immediately patch up the damage to save the tissue. But, the scar they form is tough and non-contractile meaning the heart’s pumping function is compromised, which can ultimately result in its failure. To improve outcomes of patients after heart attacks, scientists are investigating in mice ways to reprogram the fibroblasts into muscle. The problem is, adult fibroblasts are particularly reluctant to change – in part, it seems, because of a transcription factor called Epas1 (stained red). But, a cocktail of RNA molecules that block Epas1 and promote muscle identity seems to do the trick. When scientists packaged this cocktail into membrane-bound droplets (called exosomes) and delivered them to the injured hearts of mice, the fibroblasts reprogrammed, scarring was reduced and heart function improved. If such an approach can be adapted for humans, it may help to maintain heart function and prolong life after a heart attack.

Written by Ruth WIlliams

Image from work by Hualing Sun and colleagues

Mandel Center for Heart and Vascular Research, and the Duke Cardiovascular Research Center, Duke University Medical Center, Durham, NC, USA

Image originally published with a Creative Commons Attribution 4.0 International (CC BY 4.0)

Published in Journal of Biological Chemistry, April 2023

You can also follow BPoD on Instagram, Twitter and Facebook

[medicomunicare]

Aminoacids and fats meet for "malignant" purposes: reexploring antipsychotic drugs paving the way for metabolic wreck

Glioblastoma (GBM) is the most lethal brain tumor, with a median survival rate of merely 12-16 months after diagnosis. Despite surgical, radiation and chemotherapy treatments, the two-year survival rate for GBM patients is less than 10%. Two major challenges hinder effective treatment: the limited penetration of anti-tumor drugs into GBM tissues because of the blood-brain-barrier; and the rapid…

[phosphorescentspaceman]

are you being quizzed on embryogenesis?

partly!! you may actually be totally right because i don't think the pictures i showed have anything other than embryogenesis terms, but I'm studying the whole developmental biology suite of content, ranging from evolutionary influences to development disorders and embryogenesis! not sure when other countries have there end of year exams, but in Australia we have them roughly now! this one is my last exam for the year <3

[tenth-sentence]

JAZ repressors also maintain the chromatin in a "closed" state that prevents JA-responsive transcription factors from binding to their agents.

"Plant Physiology and Development" int'l 6e - Taiz, L., Zeiger, E., Møller, I.M., Murphy, A.

[whats-in-a-sentence]

TRY is expressed in developing trichomes and moves to the surrounding cells, where it inactivates the GL1-GL3-TTG1 complex by displacing GL1 (Figure 19.14). (...) GL2, which is activated in trichome cells by the GL1-GL3-TTG1 complex, encodes a homeodomain leucine zipper transcription factor (see Figure 19.14). (...) Also, jasmonic acid participates in trichome initiation by degrading JAZ proteins, thereby abolishing the interactions of JAZ proteins with bHLH and MYB factors, which activate the transcription of trichome activators (see Figure 19.14).

"Plant Physiology and Development" int'l 6e - Taiz, L., Zeiger, E., Møller, I.M., Murphy, A.