Mohamed Asif

Project Associate @IITMadras

Passionate about Natural Product-Based Drug Discovery 🌿🔬, Cancer Biology.

Exploring Microfluidics 🔍

[Varun Krishnan @varunkrish]

Crazy experience with TNEB. Been trying for name transfer since 2010 for 16 yrs. They sent me back 5 times citing some documents and💰
Applied online on official site on Aug 1st , completed on Aug 6th! Paid some 500rs fees and never visited their office. Unbelievable!

[Ram Krishna @nanasaiin]

Tamil a cultural blind spot for AI models @dt_next

#Tamil #AI #Tamillanguage

https://t.co/DGoFZxwOkJ

[Mohamed Asif @asifadil86]

Do we all get the same amount of life? A mayfly lives one day; a tortoise lives a century. But what if they experience the same amount of subjective time?

TIME PERCEPTION explores the biological clocks that govern reality. Seeking rep for my pop-science book, TIME PERCEPTION. #MSWL #amquerying

[Mohamed Asif @asifadil86]

Silver in my hair,
but gold in these quiet rooms
Sheltered by their love.
Every shared smile is a treasure,
every quiet moment, a lifetime of love.

[Mohamed Asif @asifadil86]

@ajay_2512x Sounds interesting 🤩, but how to reach you out guys. 🤨

[Mohamed Asif @asifadil86]

My Sunday rabbit hole led me to something completely outside this framework.

We're already pushing past the standard A-T-C-G. Expanded genetic alphabets, orthogonal translation systems, non-natural amino acids, and even "Mirror Life" are attempting to synthesise reverse chirality systems.

But are we just tweaking the existing code? If we look beyond the framework of DNA, RNA, and proteins entirely... what entirely different paradigms of life are theoretically possible?

What lies beyond the standard biological model? Let’s discuss.

#Biology #SyntheticBiology #CentralDogma #MirrorLife #FutureOfScience

[Mohamed Asif @asifadil86]

Finding a potential drug for pancreatic cancer is a needle in a haystack problem, but we might have just found it. 🧬

Proud to share our latest research where we took 189K compounds and narrowed them down to highly stable, targeted natural leads that successfully inhibit KRAS G12D in vitro in PDAC models. If these early stability profiles hold up, we could be looking at a completely new therapeutic avenue.

Read the full study via @SpringerNature : https://t.co/K0HXliXIyv

Hoping these findings contribute to the ongoing efforts of the @AACR and @PanCAN communities! @AcademicChatter @OncoAlert

#KRASG12D #PDAC #TargetedTherapy #PancreaticCancer #Mangiferin #NaturalProduct

[Mohamed Asif @asifadil86]

@OdedRechavi Don't tell the In Silico crowd that.

They’ve already got the clusters warming up and the 'Novel Inhibitor' templates half-written.

[Mohamed Asif @asifadil86]

@demirbasayyuce I don't usually recommend using AI, but during last-minute chaos, Claude can help you put together a presentation. 😉

[Cliff Pickover @pickover]

“Reality in Layers.” The Stratified Cosmos.

I created this diagram, stimulated by https://t.co/tN8v8WAmSV

[Mohamed Asif @asifadil86]

@nitesh_singh5 Interested

[Mohamed Asif @asifadil86]

Weekends are meant for turning paper concepts into Python code. ☕

Simulating a 3-channel μPAD for HPV detection. It models capillary flow (Lucas-Washburn physics) and LAMP reaction kinetics for detecting HPV 16 & 18.
https://t.co/DYulyaXcNJ

#Microfluidics #OpenScience #HPV

[Mohamed Asif @asifadil86]

Thursday group meeting at PRL is a wrap with Prof. Pushpavanam. I presented on the rapid detection of HPV 16 & 18 using paper-based microfluidic devices
The highlight? Somehow managing to make Chemical Engineers understand viral-mediated carcinogenesis, DNA, PCR, and LAMP!
#IITM

[Goldy Dev @golldyydev]

We need to do hard things at least once in our lives to become extraordinary. Everything is hard — content creation, the gym, studying. The people who consistently do the hard things end up living the easiest lives later on, or at least it looks that way to others.

Or if I say in Washir Badra sahab langugage -

"Yeh phool mujhe koi virasat mein nahi mile,
Tumne mera kaanton bhara bistar nahi dekha."

[Mohamed Asif @asifadil86]

When the Chennai rains turn the street into a river and your auto driver starts charging cruise ship rates. 🚢💸
Still, gotta love the adventure!

#ChennaiRains #chennai #autorides

[Mohamed Asif @asifadil86]

@JSheltzer Hi Prof Sheltzer,
Your lab's work on cancer therapeutics is amazing! I'm an international candidate from India and wanted to quickly check if you might have a PhD position available, and if you accept international applicants? Thanks!

[Mohamed Asif @asifadil86]

@AbhishekDGarg @KU_Leuven @UZLeuven This is an amazing opportunity. I'd love to be a part of your team. Will you consider accepting international candidates for this position?

[Mohamed Asif @asifadil86]

@mkstalin Looks like Vijay and TVK have set the benchmark 👀🔥"

Earlier, this wasn’t even a trend. Now they’re padding rallies with paid crowds just to ‘show off.

Are you scared, rivals?
#DMK etc...

[Niko McCarty. @NikoMcCarty]

A single E. coli cell, placed on a dish, will become 70 billion cells in just 12 hours. That’s exponential growth.

But a new preprint shows that it's possible to engineer E. coli to grow linearly instead, where only one daughter cell continues dividing and the other stops.

First, some context. In nature, there is a bacterium called Mycobacterium smegmatis (initially discovered in 1884 in ulcers scraped from syphilis patients.) M. smegmatis is weird because it divides asymmetrically. These cells grow only from one end, and all their cell wall biosynthesis machinery is located on that one end. So when the cell divides, one daughter gets this machinery and the other gets nothing. The daughter that gets the machinery can keep dividing immediately, but the other daughter has to remake all that machinery from scratch, so its growth is delayed.

E. coli doesn’t grow like this. When it divides, it pinches in the middle and splits everything evenly. Enzymes, metabolites, and proteins get partitioned more or less randomly between the two daughters.

For the new preprint, though, researchers engineered E. coli to behave more like M. smegmatis. Here is how they did it:

First, they deleted a gene called cyaA, which encodes an enzyme (adenylate cyclase) that makes a molecule called cAMP.

cAMP is SUPER IMPORTANT! It is a nutrient sensor that instructs E. coli to switch on genes that help it digest non-glucose carbon sources when glucose is scarce. Without cAMP, E. coli cells growing on alternative carbon sources will starve; they won’t know how to eat the food.

Next, they added back a “split” version of the cyaA gene into the cells. In other words, they split the gene in two so that each half of the enzyme is made separately. Cells can only make cAMP, and thus eat non-glucose carbon sources, if these two halves come together.

To facilitate that “coming together,” the researchers also fused the split cyaA proteins to sticky proteins that clump together, and to a fluorescent protein (to make it easy to track these molecules in the cell.)

So now some interesting things start to happen if you grow E. coli on a growth medium lacking glucose.

As the cell grows, its cyaA “halves” start clumping together into a giant ball. Inside the aggregate, the two enzyme halves come together and make cAMP. And when the cell gets big enough and divides, the clump of cyaA RANDOMLY goes to either daughter cell #1 or #2.

The daughter that gets the aggregate (called PA+ in this paper) can keep dividing. The daughter that doesn’t (PA–) cannot. It still grows a few times — about four divisions — because it inherits some leftover cAMP from its mother. But after that, the metabolite is diluted away, and the cell stops growing.

PA+ cells went through about 23 divisions on average before their aggregate decayed. And the population of cells, as a whole, grew linearly.

This paper is cool because there are many applications where exponential growth is too unpredictable and, perhaps, unsafe. If you want to engineer bacteria to deliver drugs, clean up waste, or live in the gut, you don’t want them to double uncontrollably. This paper shows you can make them expand in a controlled, linear way.

Alas, mutations could break this whole engineered system. A mutation that restores cyaA, for example, would give cells a new way to make cAMP. Mutations that make the aggregates split between daughters would break the asymmetry, too. But still, I really enjoy proof-of-concept engineering papers like this.