Toolkit/MALAT1
MALAT1
Taxonomy: Mechanism Branch / Component. Workflows sit above the mechanism and technique branches rather than replacing them.
Summary
MALAT1 is a long noncoding RNA reported in trophoblasts to promote cell migration and invasion by reducing CRY2 protein abundance. In the cited study, MALAT1 recruits the E3 ubiquitin ligase FBXW7, impairing CRY2 protein stability and inducing ubiquitin-mediated CRY2 degradation.
Usefulness & Problems
Why this is useful
This RNA element is useful as a mechanistic regulator linking a lncRNA to post-translational control of CRY2 in trophoblast biology. It provides a reported means to modulate trophoblast migration and invasion through FBXW7-dependent protein degradation.
Source:
MALAT1 promoted trophoblast cell migration and invasion by negatively regulating CRY2 protein expression.
Problem solved
The cited work addresses how MALAT1 can influence trophoblast migration and invasion at the molecular level. Specifically, it proposes that MALAT1 solves this regulatory task by recruiting FBXW7 to destabilize CRY2 and promote its ubiquitin-mediated degradation.
Problem links
Need conditional protein clearance
DerivedMALAT1 is a long noncoding RNA reported to promote trophoblast migration and invasion by negatively regulating CRY2 protein expression. In the cited study, MALAT1 recruits the E3 ubiquitin ligase FBXW7 to impair CRY2 protein stability and induce CRY2 ubiquitin-mediated degradation.
Need conditional recombination or state switching
DerivedMALAT1 is a long noncoding RNA reported to promote trophoblast migration and invasion by negatively regulating CRY2 protein expression. In the cited study, MALAT1 recruits the E3 ubiquitin ligase FBXW7 to impair CRY2 protein stability and induce CRY2 ubiquitin-mediated degradation.
Taxonomy & Function
Primary hierarchy
Mechanism Branch
Component: A low-level RNA part used inside a larger architecture that realizes a mechanism.
Mechanisms
DegradationDegradatione3 ligase recruitmente3 ligase recruitmentnegative regulation of protein stabilitynegative regulation of protein stabilityubiquitin-mediated protein degradationubiquitin-mediated protein degradationTechniques
No technique tags yet.
Target processes
degradationrecombinationImplementation Constraints
Practical implementation details are sparse in the supplied evidence. What is known is that the reported activity depends on endogenous or introduced MALAT1 acting in a context where FBXW7 and CRY2 are present, but no construct design, delivery method, expression system, or cofactor requirements are described here.
Evidence is limited to a single cited study in trophoblast and villous specimen contexts, with no independent replication provided here. The supplied evidence does not define sequence features, structural determinants, portability to other systems, or any role in recombination despite that target process being listed.
Validation
Observations
Inferred from claim c2 during normalization. MALAT1 promotes trophoblast cell migration and invasion by negatively regulating CRY2 protein expression. Derived from claim c2. Quoted text: MALAT1 promoted trophoblast cell migration and invasion by negatively regulating CRY2 protein expression.
Source:
Inferred from claim c2 during normalization. MALAT1 promotes trophoblast cell migration and invasion by negatively regulating CRY2 protein expression. Derived from claim c2. Quoted text: MALAT1 promoted trophoblast cell migration and invasion by negatively regulating CRY2 protein expression.
Source:
Inferred from claim c2 during normalization. MALAT1 promotes trophoblast cell migration and invasion by negatively regulating CRY2 protein expression. Derived from claim c2. Quoted text: MALAT1 promoted trophoblast cell migration and invasion by negatively regulating CRY2 protein expression.
Source:
Inferred from claim c2 during normalization. MALAT1 promotes trophoblast cell migration and invasion by negatively regulating CRY2 protein expression. Derived from claim c2. Quoted text: MALAT1 promoted trophoblast cell migration and invasion by negatively regulating CRY2 protein expression.
Source:
Inferred from claim c2 during normalization. MALAT1 promotes trophoblast cell migration and invasion by negatively regulating CRY2 protein expression. Derived from claim c2. Quoted text: MALAT1 promoted trophoblast cell migration and invasion by negatively regulating CRY2 protein expression.
Source:
Inferred from claim c2 during normalization. MALAT1 promotes trophoblast cell migration and invasion by negatively regulating CRY2 protein expression. Derived from claim c2. Quoted text: MALAT1 promoted trophoblast cell migration and invasion by negatively regulating CRY2 protein expression.
Source:
Inferred from claim c2 during normalization. MALAT1 promotes trophoblast cell migration and invasion by negatively regulating CRY2 protein expression. Derived from claim c2. Quoted text: MALAT1 promoted trophoblast cell migration and invasion by negatively regulating CRY2 protein expression.
Source:
Supporting Sources
Ranked Claims
MALAT1 downregulation in trophoblasts might be related to miscarriage.
MALAT1 downregulation in trophoblasts might be related to miscarriage.
MALAT1 downregulation in trophoblasts might be related to miscarriage.
MALAT1 downregulation in trophoblasts might be related to miscarriage.
MALAT1 downregulation in trophoblasts might be related to miscarriage.
MALAT1 downregulation in trophoblasts might be related to miscarriage.
MALAT1 downregulation in trophoblasts might be related to miscarriage.
MALAT1 downregulation in trophoblasts might be related to miscarriage.
MALAT1 downregulation in trophoblasts might be related to miscarriage.
MALAT1 downregulation in trophoblasts might be related to miscarriage.
MALAT1 downregulation in trophoblasts might be related to miscarriage.
MALAT1 downregulation in trophoblasts might be related to miscarriage.
MALAT1 downregulation in trophoblasts might be related to miscarriage.
MALAT1 downregulation in trophoblasts might be related to miscarriage.
MALAT1 downregulation in trophoblasts might be related to miscarriage.
MALAT1 downregulation in trophoblasts might be related to miscarriage.
MALAT1 downregulation in trophoblasts might be related to miscarriage.
MALAT1 downregulation in trophoblasts might be related to miscarriage.
MALAT1 downregulation in trophoblasts might be related to miscarriage.
MALAT1 downregulation in trophoblasts might be related to miscarriage.
MALAT1 downregulation in trophoblasts might be related to miscarriage.
MALAT1 downregulation in trophoblasts might be related to miscarriage.
MALAT1 downregulation in trophoblasts might be related to miscarriage.
MALAT1 downregulation in trophoblasts might be related to miscarriage.
MALAT1 downregulation in trophoblasts might be related to miscarriage.
MALAT1 downregulation in trophoblasts might be related to miscarriage.
MALAT1 downregulation in trophoblasts might be related to miscarriage.
MALAT1 downregulation in trophoblasts might be related to miscarriage.
MALAT1 downregulation in trophoblasts might be related to miscarriage.
MALAT1 downregulation in trophoblasts might be related to miscarriage.
MALAT1 downregulation in trophoblasts might be related to miscarriage.
MALAT1 downregulation in trophoblasts might be related to miscarriage.
MALAT1 downregulation in trophoblasts might be related to miscarriage.
MALAT1 downregulation in trophoblasts might be related to miscarriage.
MALAT1 expression is decreased in villous specimens from recurrent spontaneous abortion patients relative to missed abortion patients and normal villous specimens.
The results showed significantly decreased MALAT1 expression in the villous specimens from the RSA patients relative to that in the villous specimens from the missed abortion patients and the normal villous specimens.
MALAT1 expression is decreased in villous specimens from recurrent spontaneous abortion patients relative to missed abortion patients and normal villous specimens.
The results showed significantly decreased MALAT1 expression in the villous specimens from the RSA patients relative to that in the villous specimens from the missed abortion patients and the normal villous specimens.
MALAT1 expression is decreased in villous specimens from recurrent spontaneous abortion patients relative to missed abortion patients and normal villous specimens.
The results showed significantly decreased MALAT1 expression in the villous specimens from the RSA patients relative to that in the villous specimens from the missed abortion patients and the normal villous specimens.
MALAT1 expression is decreased in villous specimens from recurrent spontaneous abortion patients relative to missed abortion patients and normal villous specimens.
The results showed significantly decreased MALAT1 expression in the villous specimens from the RSA patients relative to that in the villous specimens from the missed abortion patients and the normal villous specimens.
MALAT1 expression is decreased in villous specimens from recurrent spontaneous abortion patients relative to missed abortion patients and normal villous specimens.
The results showed significantly decreased MALAT1 expression in the villous specimens from the RSA patients relative to that in the villous specimens from the missed abortion patients and the normal villous specimens.
MALAT1 expression is decreased in villous specimens from recurrent spontaneous abortion patients relative to missed abortion patients and normal villous specimens.
The results showed significantly decreased MALAT1 expression in the villous specimens from the RSA patients relative to that in the villous specimens from the missed abortion patients and the normal villous specimens.
MALAT1 expression is decreased in villous specimens from recurrent spontaneous abortion patients relative to missed abortion patients and normal villous specimens.
The results showed significantly decreased MALAT1 expression in the villous specimens from the RSA patients relative to that in the villous specimens from the missed abortion patients and the normal villous specimens.
MALAT1 expression is decreased in villous specimens from recurrent spontaneous abortion patients relative to missed abortion patients and normal villous specimens.
The results showed significantly decreased MALAT1 expression in the villous specimens from the RSA patients relative to that in the villous specimens from the missed abortion patients and the normal villous specimens.
MALAT1 expression is decreased in villous specimens from recurrent spontaneous abortion patients relative to missed abortion patients and normal villous specimens.
The results showed significantly decreased MALAT1 expression in the villous specimens from the RSA patients relative to that in the villous specimens from the missed abortion patients and the normal villous specimens.
MALAT1 expression is decreased in villous specimens from recurrent spontaneous abortion patients relative to missed abortion patients and normal villous specimens.
The results showed significantly decreased MALAT1 expression in the villous specimens from the RSA patients relative to that in the villous specimens from the missed abortion patients and the normal villous specimens.
MALAT1 expression is decreased in villous specimens from recurrent spontaneous abortion patients relative to missed abortion patients and normal villous specimens.
The results showed significantly decreased MALAT1 expression in the villous specimens from the RSA patients relative to that in the villous specimens from the missed abortion patients and the normal villous specimens.
MALAT1 expression is decreased in villous specimens from recurrent spontaneous abortion patients relative to missed abortion patients and normal villous specimens.
The results showed significantly decreased MALAT1 expression in the villous specimens from the RSA patients relative to that in the villous specimens from the missed abortion patients and the normal villous specimens.
MALAT1 expression is decreased in villous specimens from recurrent spontaneous abortion patients relative to missed abortion patients and normal villous specimens.
The results showed significantly decreased MALAT1 expression in the villous specimens from the RSA patients relative to that in the villous specimens from the missed abortion patients and the normal villous specimens.
MALAT1 expression is decreased in villous specimens from recurrent spontaneous abortion patients relative to missed abortion patients and normal villous specimens.
The results showed significantly decreased MALAT1 expression in the villous specimens from the RSA patients relative to that in the villous specimens from the missed abortion patients and the normal villous specimens.
MALAT1 expression is decreased in villous specimens from recurrent spontaneous abortion patients relative to missed abortion patients and normal villous specimens.
The results showed significantly decreased MALAT1 expression in the villous specimens from the RSA patients relative to that in the villous specimens from the missed abortion patients and the normal villous specimens.
MALAT1 expression is decreased in villous specimens from recurrent spontaneous abortion patients relative to missed abortion patients and normal villous specimens.
The results showed significantly decreased MALAT1 expression in the villous specimens from the RSA patients relative to that in the villous specimens from the missed abortion patients and the normal villous specimens.
MALAT1 expression is decreased in villous specimens from recurrent spontaneous abortion patients relative to missed abortion patients and normal villous specimens.
The results showed significantly decreased MALAT1 expression in the villous specimens from the RSA patients relative to that in the villous specimens from the missed abortion patients and the normal villous specimens.
MALAT1 promotes trophoblast cell migration and invasion by negatively regulating CRY2 protein expression.
MALAT1 promoted trophoblast cell migration and invasion by negatively regulating CRY2 protein expression.
MALAT1 promotes trophoblast cell migration and invasion by negatively regulating CRY2 protein expression.
MALAT1 promoted trophoblast cell migration and invasion by negatively regulating CRY2 protein expression.
MALAT1 promotes trophoblast cell migration and invasion by negatively regulating CRY2 protein expression.
MALAT1 promoted trophoblast cell migration and invasion by negatively regulating CRY2 protein expression.
MALAT1 promotes trophoblast cell migration and invasion by negatively regulating CRY2 protein expression.
MALAT1 promoted trophoblast cell migration and invasion by negatively regulating CRY2 protein expression.
MALAT1 promotes trophoblast cell migration and invasion by negatively regulating CRY2 protein expression.
MALAT1 promoted trophoblast cell migration and invasion by negatively regulating CRY2 protein expression.
MALAT1 promotes trophoblast cell migration and invasion by negatively regulating CRY2 protein expression.
MALAT1 promoted trophoblast cell migration and invasion by negatively regulating CRY2 protein expression.
MALAT1 promotes trophoblast cell migration and invasion by negatively regulating CRY2 protein expression.
MALAT1 promoted trophoblast cell migration and invasion by negatively regulating CRY2 protein expression.
MALAT1 promotes trophoblast cell migration and invasion by negatively regulating CRY2 protein expression.
MALAT1 promoted trophoblast cell migration and invasion by negatively regulating CRY2 protein expression.
MALAT1 promotes trophoblast cell migration and invasion by negatively regulating CRY2 protein expression.
MALAT1 promoted trophoblast cell migration and invasion by negatively regulating CRY2 protein expression.
MALAT1 promotes trophoblast cell migration and invasion by negatively regulating CRY2 protein expression.
MALAT1 promoted trophoblast cell migration and invasion by negatively regulating CRY2 protein expression.
MALAT1 promotes trophoblast cell migration and invasion by negatively regulating CRY2 protein expression.
MALAT1 promoted trophoblast cell migration and invasion by negatively regulating CRY2 protein expression.
MALAT1 promotes trophoblast cell migration and invasion by negatively regulating CRY2 protein expression.
MALAT1 promoted trophoblast cell migration and invasion by negatively regulating CRY2 protein expression.
MALAT1 promotes trophoblast cell migration and invasion by negatively regulating CRY2 protein expression.
MALAT1 promoted trophoblast cell migration and invasion by negatively regulating CRY2 protein expression.
MALAT1 promotes trophoblast cell migration and invasion by negatively regulating CRY2 protein expression.
MALAT1 promoted trophoblast cell migration and invasion by negatively regulating CRY2 protein expression.
MALAT1 promotes trophoblast cell migration and invasion by negatively regulating CRY2 protein expression.
MALAT1 promoted trophoblast cell migration and invasion by negatively regulating CRY2 protein expression.
MALAT1 promotes trophoblast cell migration and invasion by negatively regulating CRY2 protein expression.
MALAT1 promoted trophoblast cell migration and invasion by negatively regulating CRY2 protein expression.
MALAT1 promotes trophoblast cell migration and invasion by negatively regulating CRY2 protein expression.
MALAT1 promoted trophoblast cell migration and invasion by negatively regulating CRY2 protein expression.
MALAT1 may recruit the E3 ubiquitin ligase FBXW7 to induce CRY2 ubiquitin-mediated degradation.
MALAT1 may recruit the E3 ubiquitin ligase FBXW7 to induce CRY2 ubiquitin-mediated degradation
MALAT1 may recruit the E3 ubiquitin ligase FBXW7 to induce CRY2 ubiquitin-mediated degradation.
MALAT1 may recruit the E3 ubiquitin ligase FBXW7 to induce CRY2 ubiquitin-mediated degradation
MALAT1 may recruit the E3 ubiquitin ligase FBXW7 to induce CRY2 ubiquitin-mediated degradation.
MALAT1 may recruit the E3 ubiquitin ligase FBXW7 to induce CRY2 ubiquitin-mediated degradation
MALAT1 may recruit the E3 ubiquitin ligase FBXW7 to induce CRY2 ubiquitin-mediated degradation.
MALAT1 may recruit the E3 ubiquitin ligase FBXW7 to induce CRY2 ubiquitin-mediated degradation
MALAT1 may recruit the E3 ubiquitin ligase FBXW7 to induce CRY2 ubiquitin-mediated degradation.
MALAT1 may recruit the E3 ubiquitin ligase FBXW7 to induce CRY2 ubiquitin-mediated degradation
MALAT1 may recruit the E3 ubiquitin ligase FBXW7 to induce CRY2 ubiquitin-mediated degradation.
MALAT1 may recruit the E3 ubiquitin ligase FBXW7 to induce CRY2 ubiquitin-mediated degradation
MALAT1 may recruit the E3 ubiquitin ligase FBXW7 to induce CRY2 ubiquitin-mediated degradation.
MALAT1 may recruit the E3 ubiquitin ligase FBXW7 to induce CRY2 ubiquitin-mediated degradation
MALAT1 may recruit the E3 ubiquitin ligase FBXW7 to induce CRY2 ubiquitin-mediated degradation.
MALAT1 may recruit the E3 ubiquitin ligase FBXW7 to induce CRY2 ubiquitin-mediated degradation
MALAT1 may recruit the E3 ubiquitin ligase FBXW7 to induce CRY2 ubiquitin-mediated degradation.
MALAT1 may recruit the E3 ubiquitin ligase FBXW7 to induce CRY2 ubiquitin-mediated degradation
MALAT1 may recruit the E3 ubiquitin ligase FBXW7 to induce CRY2 ubiquitin-mediated degradation.
MALAT1 may recruit the E3 ubiquitin ligase FBXW7 to induce CRY2 ubiquitin-mediated degradation
MALAT1 may recruit the E3 ubiquitin ligase FBXW7 to induce CRY2 ubiquitin-mediated degradation.
MALAT1 may recruit the E3 ubiquitin ligase FBXW7 to induce CRY2 ubiquitin-mediated degradation
MALAT1 may recruit the E3 ubiquitin ligase FBXW7 to induce CRY2 ubiquitin-mediated degradation.
MALAT1 may recruit the E3 ubiquitin ligase FBXW7 to induce CRY2 ubiquitin-mediated degradation
MALAT1 may recruit the E3 ubiquitin ligase FBXW7 to induce CRY2 ubiquitin-mediated degradation.
MALAT1 may recruit the E3 ubiquitin ligase FBXW7 to induce CRY2 ubiquitin-mediated degradation
MALAT1 may recruit the E3 ubiquitin ligase FBXW7 to induce CRY2 ubiquitin-mediated degradation.
MALAT1 may recruit the E3 ubiquitin ligase FBXW7 to induce CRY2 ubiquitin-mediated degradation
MALAT1 may recruit the E3 ubiquitin ligase FBXW7 to induce CRY2 ubiquitin-mediated degradation.
MALAT1 may recruit the E3 ubiquitin ligase FBXW7 to induce CRY2 ubiquitin-mediated degradation
MALAT1 may recruit the E3 ubiquitin ligase FBXW7 to induce CRY2 ubiquitin-mediated degradation.
MALAT1 may recruit the E3 ubiquitin ligase FBXW7 to induce CRY2 ubiquitin-mediated degradation
MALAT1 may recruit the E3 ubiquitin ligase FBXW7 to induce CRY2 ubiquitin-mediated degradation.
MALAT1 may recruit the E3 ubiquitin ligase FBXW7 to induce CRY2 ubiquitin-mediated degradation
MALAT1 recruits FBXW7 to impair CRY2 protein stability.
MALAT1 recruited FBXW7 to impair CRY2 protein stability.
MALAT1 recruits FBXW7 to impair CRY2 protein stability.
MALAT1 recruited FBXW7 to impair CRY2 protein stability.
MALAT1 recruits FBXW7 to impair CRY2 protein stability.
MALAT1 recruited FBXW7 to impair CRY2 protein stability.
MALAT1 recruits FBXW7 to impair CRY2 protein stability.
MALAT1 recruited FBXW7 to impair CRY2 protein stability.
MALAT1 recruits FBXW7 to impair CRY2 protein stability.
MALAT1 recruited FBXW7 to impair CRY2 protein stability.
MALAT1 recruits FBXW7 to impair CRY2 protein stability.
MALAT1 recruited FBXW7 to impair CRY2 protein stability.
MALAT1 recruits FBXW7 to impair CRY2 protein stability.
MALAT1 recruited FBXW7 to impair CRY2 protein stability.
MALAT1 recruits FBXW7 to impair CRY2 protein stability.
MALAT1 recruited FBXW7 to impair CRY2 protein stability.
MALAT1 recruits FBXW7 to impair CRY2 protein stability.
MALAT1 recruited FBXW7 to impair CRY2 protein stability.
MALAT1 recruits FBXW7 to impair CRY2 protein stability.
MALAT1 recruited FBXW7 to impair CRY2 protein stability.
MALAT1 recruits FBXW7 to impair CRY2 protein stability.
MALAT1 recruited FBXW7 to impair CRY2 protein stability.
MALAT1 recruits FBXW7 to impair CRY2 protein stability.
MALAT1 recruited FBXW7 to impair CRY2 protein stability.
MALAT1 recruits FBXW7 to impair CRY2 protein stability.
MALAT1 recruited FBXW7 to impair CRY2 protein stability.
MALAT1 recruits FBXW7 to impair CRY2 protein stability.
MALAT1 recruited FBXW7 to impair CRY2 protein stability.
MALAT1 recruits FBXW7 to impair CRY2 protein stability.
MALAT1 recruited FBXW7 to impair CRY2 protein stability.
MALAT1 recruits FBXW7 to impair CRY2 protein stability.
MALAT1 recruited FBXW7 to impair CRY2 protein stability.
MALAT1 recruits FBXW7 to impair CRY2 protein stability.
MALAT1 recruited FBXW7 to impair CRY2 protein stability.
Approval Evidence
MALAT1
Source:
MALAT1 downregulation in trophoblasts might be related to miscarriage.
MALAT1 downregulation in trophoblasts might be related to miscarriage.
Source:
MALAT1 expression is decreased in villous specimens from recurrent spontaneous abortion patients relative to missed abortion patients and normal villous specimens.
The results showed significantly decreased MALAT1 expression in the villous specimens from the RSA patients relative to that in the villous specimens from the missed abortion patients and the normal villous specimens.
Source:
MALAT1 promotes trophoblast cell migration and invasion by negatively regulating CRY2 protein expression.
MALAT1 promoted trophoblast cell migration and invasion by negatively regulating CRY2 protein expression.
Source:
MALAT1 may recruit the E3 ubiquitin ligase FBXW7 to induce CRY2 ubiquitin-mediated degradation.
MALAT1 may recruit the E3 ubiquitin ligase FBXW7 to induce CRY2 ubiquitin-mediated degradation
Source:
MALAT1 recruits FBXW7 to impair CRY2 protein stability.
MALAT1 recruited FBXW7 to impair CRY2 protein stability.
Source:
Comparisons
Source-backed strengths
The available evidence specifies a named substrate-ligase axis, FBXW7-CRY2, rather than only a correlative phenotype. The study also connects this mechanism to a cellular outcome, reporting that MALAT1 promotes trophoblast migration and invasion and is decreased in villous specimens from recurrent spontaneous abortion patients.
Compared with blue light-responsive Cas13b mRNA knockdown system
MALAT1 and blue light-responsive Cas13b mRNA knockdown system address a similar problem space because they share degradation.
Shared frame: same top-level item type; shared target processes: degradation; shared mechanisms: degradation
Strengths here: looks easier to implement in practice.
Compared with PCB synthesis expression vector
MALAT1 and PCB synthesis expression vector address a similar problem space because they share degradation, recombination.
Shared frame: shared target processes: degradation, recombination; shared mechanisms: degradation
Strengths here: looks easier to implement in practice; may avoid an exogenous cofactor requirement.
Compared with synthetically engineered guide RNA
MALAT1 and synthetically engineered guide RNA address a similar problem space because they share degradation, recombination.
Shared frame: same top-level item type; shared target processes: degradation, recombination; shared mechanisms: degradation
Ranked Citations
- 1.